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Does The Sympathetic Nervous System Increase or Decrease Urination?

Does The Sympathetic Nervous System Increase or Decrease Urination?


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According to my book:

Sympathetic nervous system stimulation, leads to the release of Norepinephrine(Noradrenaline), priming the body for the "Fight or Flight" response.

It is also stated that:

The effect of sympathetic stimulation is to maintain urinary continence.

But if sympathetic stimulation results in urinary continence, why do we urinate more when afraid or nervous?


I've read this quesion, but the accepted answer states that adernaline(epinephrine) is released (not norepinephrine) and doesn't provide evidence to support why does adernaline result in more urination.


What is the role of the sympathetic nervous system in the neuroanatomy of neurogenic bladder?

When the sympathetic nervous system is active, it causes the bladder to increase its capacity without increasing detrusor resting pressure (accommodation) and stimulates the internal urinary sphincter to remain tightly closed. The sympathetic activity also inhibits parasympathetic stimulation, preventing bladder contractions. When the sympathetic nervous system is active, urinary accommodation occurs and the micturition reflex is suppressed.

Related Questions:

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Tables

Contributor Information and Disclosures

Bradley C Gill, MD, MS Chief Resident, Department of Urology, Glickman Urological and Kidney Institute Clinical Instructor of Surgery, Cleveland Clinic Lerner College of Medicine, Education Institute Consulting Staff, Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic

Disclosure: Nothing to disclose.

Sandip P Vasavada, MD Associate Professor of Surgery, Cleveland Clinic Lerner College of Medicine Physician, Center for Female Urology and Genitourinary Reconstructive Surgery, The Glickman Urological and Kidney Institute Joint Appointment with Women's Institute, Cleveland Clinic

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Medtronic, Axonics, BlueWind<br/>Received ownership interest from NDI Medical, LLC for review panel membership Received consulting fee from allergan for speaking and teaching Received consulting fee from medtronic for speaking and teaching Received consulting fee from boston scientific for consulting. for: Oasis Consumer Healthcare.

Farzeen Firoozi, MD Clinical Fellow, Center for Female Urology and Pelvic Reconstructive Surgery, Glickman Urological Institute, Cleveland Clinic Foundation

Farzeen Firoozi, MD is a member of the following medical societies: American Medical Association, American Urological Association

Disclosure: Nothing to disclose.

Raymond R Rackley, MD Professor of Surgery, Cleveland Clinic Lerner College of Medicine Staff Physician, Center for Neurourology, Female Pelvic Health and Female Reconstructive Surgery, Glickman Urological Institute, Cleveland Clinic, Beachwood Family Health Center, and Willoughby Hills Family Health Center Director, The Urothelial Biology Laboratory, Lerner Research Institute, Cleveland Clinic

Raymond R Rackley, MD is a member of the following medical societies: American Urological Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Edward David Kim, MD, FACS Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine Consulting Staff, University of Tennessee Medical Center

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Endo.

Raymond R Rackley, MD Professor of Surgery, Cleveland Clinic Lerner College of Medicine Staff Physician, Center for Neurourology, Female Pelvic Health and Female Reconstructive Surgery, Glickman Urological Institute, Cleveland Clinic, Beachwood Family Health Center, and Willoughby Hills Family Health Center Director, The Urothelial Biology Laboratory, Lerner Research Institute, Cleveland Clinic

Raymond R Rackley, MD is a member of the following medical societies: American Urological Association

Disclosure: Nothing to disclose.

Shlomo Raz, MD Professor, Department of Surgery, Division of Urology, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

Michael S Ingber, MD Clinical Fellow, Glickman Urological and Kidney Institute of the Cleveland Clinic


Everything You Need to Know About Sympathetic Nervous System

How does your body respond to stressful situations? Have you ever wondered why your heart suddenly beats rapidly and you break out into a sweat when you encounter some form of danger? It's almost an automatic response that occurs whenever you sense a threat, whether it is just a potential embarrassing situation or a really scary situation such as an attack by a stranger. This fight-or-flight response is brought about by your sympathetic nervous system, which usually helps you deal with stress.

What Is the Sympathetic Nervous System?

While your brain, which is a vital part of the central nervous system, has the capability to control your conscious actions like walking, thinking and talking, your body also has an autonomic nervous system, which regulates your bodily functions, like the beating of your heart, your breathing, the way you digest your food, your sweating patterns, etc.

The autonomic system has two divisions. It consists of the sympathetic and parasympathetic nervous systems. The primary function of the sympathetic system is to stimulate your fight-or-flight response which is a physiological reaction that happens in response to a perceived harmful event, attack or threat to survival. The parasympathetic system enables you to maintain normal functions such as digesting and keeping the body at rest.

The Structure of the Sympathetic Nervous System

Transmission of signals in the system is accomplished through a network of nerve cells called neurons. There are two types of neurons: the preganglionic neurons and the postganglionic neurons. The preganglionic neurons have short fibers that originate from the spinal cord's thoracolumbar segments, which communicate with ganglia adjacent to the spinal column, and synapse with the longer postganglionic neurons.

Preganglionic neurons synapse with ganglia and release a chemical (neurotransmitter) called acetylcholine, which activates receptors on the postganglionic neurons. The postganglionic neurons in turn release a hormone called norepinephrine, which targets adrenergic receptors on various organs and tissues. Stimulation of these target receptors result in the characteristic fight-or-flight responses.

There are two exceptions to the processes mentioned above, which are the postganglionic neurons found in the sweat glands and the chromaffin cells found in the adrenal medulla. The postganglionic neurons discharge acetylcholine to activate muscarinic receptors, except for the palms, soles of the feet and other areas with thick skin. In these areas, norepinephrine acts on the adrenergic receptors. The chromaffin cells found in the adrenal medulla are equivalent to postganglionic neurons. Preganglionic neurons communicate with the chromaffin cells and stimulate them to release epinephrine and norepinephrine directly into your blood.

Two Hormones Behind the Sympathetic Nervous Activation

The sympathetic nervous system releases two hormones within the body in response to stress, resulting in an "adrenaline rush", or a sense of urgency that occurs during stressful conditions. These hormones are called epinephrine and norepinephrine, which help your body perform optimally during such events.

Upon activation of your system, norepinephrine is released to prepare the body for the initial stages of stress. If the stress is quickly resolved, the body functions return to normal. However, if the stressful event persists, your body produces epinephrine to increase these effects and activate various parts of the body to react accordingly.

What Happens If the Sympathetic Nervous Is Activated?

When one faces a dangerous or stressful situation, the sympathetic nervous system is automatically activated without conscious control. Various body functions are activated almost simultaneously such as:

  1. Stimulation of the adrenal glands to release norepinephrine and epinephrine, which are responsible for the cascade of reactions associated with stress.
  2. An increase in heart rate, which results in an increased delivery of oxygen and nutrients to the brain and the muscles to prepare them for the stress.
  3. An increase in glucose, released from the liver into the bloodstream to provide more energy to the muscles.
  4. Widening of the airways (bronchioles) in the lungs to allow more air, which increases oxygen supply to the blood and the rest of the body.
  5. Dilatation of the pupils, which is often observed when you are surprised or threatened.
  6. Slowing down of digestive activity, which helps conserve your body's energy that can be used to defend itself against stress.
  7. Relaxation of the bladder, which enables you to hold your urine while you are stressed. However, in worsening situations, some people involuntarily lose bladder control because of a crippling fear that allows their body to let go.

These are just some of the common functions involved in the fight-or-flight response regulated by your sympathetic nervous system. Because of such body reactions, your body is prepared to run, fight, lift heavy weights or react according to the need, depending on specific threatening situations. When the situation is resolved, the sympathetic functions return to its resting state, allowing your heart rate to go back to normal, your breathing to slow down, and your other body functions to return to a balanced state.


Differences Between Sympathetic And Parasympathetic Nervous System

The sympathetic and parasympathetic systems are a part of the peripheral nervous system. Here, we explain the differences between them.

The sympathetic and parasympathetic systems are a part of the peripheral nervous system. Here, we explain the differences between them.

The sympathetic and parasympathetic systems together are a part of the nervous system. They act in tandem to maintain a state of homeostasis in the body. Before we go on to understand the various responses and effects of these two systems, we need to understand where these two systems originate from.

The nervous system is divided into the central nervous system (consisting of the brain and the spinal cord) and the peripheral nervous system (consisting of nerve branches arising from the brain and spinal cord). The peripheral nervous system is further divided into the somatic and autonomic system. It is the autonomic nervous system that is divided into the sympathetic and parasympathetic nervous system.

Sympathetic Nervous System

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The sympathetic nervous system is one of the parts of the peripheral nervous system. The sympathetic nerves originate in the vertebrate column beginning in the first thoracic segment of the spinal cord, extending upwards until the second or the third lumbar segments. The main function of the sympathetic nervous system is to mobilize the body’s response under stressful circumstances. Thus, the sympathetic nervous system initializes the ‘fight or flight’ response of the body. The sympathetic system innervates many different organs of the body, such as the eyes, lungs, kidneys, gastrointestinal tract, heart, etc. It causes an increase in the heart rate and in the rate of secretions. It also increases the secretion of renin from the kidneys. There is also stimulation of release of glucose from the liver, which is released into the blood, so as to make it available for use by the body.

Parasympathetic Nervous System

The parasympathetic nervous system is a division of the autonomic nervous system. This is a part of the autonomic nervous system that is responsible for the ‘rest and digest’ phase of the body. The nerves of this system send fibers to cardiac muscles, smooth muscles, and to the glandular tissue. The parasympathetic nervous system is responsible for bringing about an increase in salivation, tear production, urination, digestion, and defecation. The basic parasympathetic system involves functions and actions that do not require an immediate reaction in the surrounding.

Difference Between Sympathetic and Parasympathetic System

There are many differences that exist, as these two systems act in an opposing manner.

Parasympathetic Nervous System: Constriction of pupils
Sympathetic Nervous System: Dilation of pupils

Parasympathetic Nervous System: Stimulation of secretion of saliva
Sympathetic Nervous System: Inhibition of secretion of saliva

Parasympathetic Nervous System: Decreases the heart rate, thus, causing a drop in the blood pressure
Sympathetic Nervous System: Increases the heart rate, thus, causing an increase in the blood pressure

Parasympathetic Nervous System: Constricts the bronchi, thus, decreasing the diameter of airway
Sympathetic Nervous System: Dilates the bronchi, thus, increasing the diameter of airway

Parasympathetic Nervous System: Stimulates activity of digestive system, like stimulation of peristalsis
Sympathetic Nervous System: Inhibits activity of the digestive system, like inhibition of peristalsis

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Parasympathetic Nervous System: Stimulates gallbladder secretions
Sympathetic Nervous System: Decreases gallbladder secretions

Parasympathetic Nervous System: Contracts urinary bladder
Sympathetic Nervous System: Relaxes urinary bladder

Parasympathetic Nervous System: Relaxes rectum
Sympathetic Nervous System: Contracts rectum

Thus, as can be inferred from the above-given table, the responses and effects of both the systems are complementary in nature, rather than being antagonistic. The sympathetic division acts as the accelerator and the parasympathetic division acts as a decelerator of the human body. Thus, these two systems try to maintain the body in a normal state of homeostasis for the maximum possible time. At a time, only one of the two systems are activated in the body depending on the type of innervation brought about and the hormones released.


The sympathetic nervous system and blood volume regulation: lessons from autonomic failure patients

Patients with autonomic failure provide a unique opportunity to study the role of sympathetic function on the regulation of blood volume. These patients have a reversal of the normal diurnal variation in urine output and have twice as much natriuresis during the night. Autonomic failure patients are also unable to conserve sodium and fail to decrease natriuresis in response to dietary sodium restriction. Whereas normal subjects are able to maintain blood pressure within narrow values throughout a wide range of plasma volumes, blood pressure is linearly correlated to changes in plasma volume in autonomic failure patients. Fludrocortisone is often used to increase plasma volume in these patients, but this effect is only transient its long-term effectiveness probably is due to potentiation of the pressor effects of norepinephrine. On the other hand, epoetin-alpha is effective in correcting the mild anemia that autonomic failure patients commonly have and improves their orthostatic hypotension in part by increasing intravascular volume. Autonomic failure patients, therefore, illustrate the role the sympathetic nervous system has in the regulation of sodium and volume. Conversely, a high salt diet induces sympathoinhibition in normal subjects. Paradoxically, sympathetic activity is increased in patients with salt-sensitive hypertension and contributes to their increase in blood pressure. Thus, in both these conditions the feedback mechanisms involving the sympathetic nervous system and volume homeostasis are impaired.


Central Mechanisms Regulating RSNA

The level of RSNA is dependent on the neuronal activity in sympathetic premotor nuclei in the brainstem and hypothalamus, including the rostral ventrolateral and ventromedial medulla [rostral ventrolateral medulla (RVLM), RVMM] and the paraventricular nucleus (PVN). The RVLM is sympatho-excitatory and plays a pivotal role in the regulation of efferent renal nerve activity. Neurons in the RVLM project to pre-ganglionic neurons in the intermediolateral cell column of the spinal cord, which via postganglionic neurons, project to peripheral organs such as heart, arteries, and kidneys (19). The remarkable reduction in blood pressure after destruction of premotor neurons in the RVLM is evidence of its important role (20). The activity of premotor neurons in the RVLM and PVN is modulated by renal mechano and chemoreceptor reflexes mediated via renal afferent nerves (4). Central and peripheral mechanisms of sympathetic regulation of the kidney are summarized in Figure 2 (19).

Figure 2. Schematic diagram of the central and peripheral mechanisms of sympathetic regulation of the heart, vessels, and kidneys. The RVLM plays a key role as a cardiovascular centre that receives and integrates peripheral signals providing information on blood pressure, fluid volume, and oxygen saturation. Instant changes in blood pressure are perceived by baroreceptors and transferred to the NTS as an input signal of baroreflex control of sympathetic outflow. Stimulation of the SFO by circulating angiotensin II increases the efferent sympathetic activity through the activation of the PVN and the RVLM neurons. Inhibitory pathways are activated between the lamina terminalis and PVN in response to plasma sodium. Increased activity of the RVLM neurons is transmitted to the intermediolateral cell column of the spinal cord, where peripheral sympathetic nerves to the heart, arteries and kidneys are activated. RVLM, rostral ventrolateral medulla NTS, nucleus tractus solitarius CVLM, caudal ventrolateral medulla PVN, paraventricular nucleus SFO, subfornical organ.

In response to an increase in blood pressure, activation of the carotid sinus and aortic depressor nerves stimulates neurons in the nucleus tractus solitarius (NTS), which project and activate neurons in the caudal ventrolateral medulla (CVLM). The neurotransmission between CVLM and RVLM is mediated by inhibitory GABAergic neurons, which suppresses neuronal activity in the RVLM, reduces sympathetic nerve activity, and thus decreases blood pressure (19). Renal afferent sensory nerves project to the RVLM via NTS and PVN, where there is integration of afferent signals from the kidney, elicited by events such as ischemia, oxidative stress, and altered angiotensin II and glucose levels. The importance of renal afferent reflexes has been demonstrated by the finding that the increase in norepinephrine secretion from the hypothalamus induced by kidney injury (21) was abolished by afferent renal denervation in rats (22).

In the brain, there are numerous neurotransmitters that modulate sympathetic nerve activity, one of these is nitric oxide (NO) that acts as both a neurotransmitter and a neuromodulator (23). Endogenous NO production, induced by neuronal NO synthase (NOS) and inducible NOS, appear to have different effects on blood pressure and sympathetic nervous system activity (24, 25). This was considered at least partly attributable to the different amount of neurotransmitter released namely sympatho-excitatory l -glutamate and inhibitory GABA within the RVLM (25). Microinjection of exogenous NO suggests cyclic 3′-5′ guanosine monophosphate-dependent mechanisms in the modulation of neuronal activity (26).

The effects of NO system activation within the central sympathetic nervous system are also mediated by the suppression of angiotensin II release. Since central angiotensin II is elevated and stimulates superoxide radical generation in cardiovascular diseases, the NO-mediated modulation of sympathetic nervous system is severely impaired in subjects with hypertension or end stage renal failure (25, 27). In Wistar Kyoto rats (WKY), overexpression of inducible NOS in the RVLM reportedly increased blood pressure, which was associated with sympathetic overactivity, and was attenuated by the antioxidant tempol (24). Inhibition of neuronal oxidative stress may, therefore, represent an effective approach to reduce neurohumoral activation in cardiovascular diseases and renal failure.


What are the effects on pain?

The nervous system, specifically the sympathetic nervous system, has been shown to be very responsive to social influences and stress. This explains why if you have a stressful week at work, or a loved one is unwell, you may find pain you may be experiencing becomes worse than normal. In some cases you may also realise that the start of your painful experiences began at a time when there were many stressful events going on in your life suggesting the pain may be more a product of the nervous system as opposed to a physical injury.

Higher than normal levels of circulating adrenaline can over time increase our sensitivity to painful stimuli and sometimes be responsible to generating pain all on its own. In this ‘wound-up’ state painful sensations can become more painful and sensations that are not normally painful can become very sore.

For example, brushing your hand off a towel to dry your hands may result in pain. This then causes you to become more worried, which in turn winds the nervous system up more, and you enter a vicious cycle: nervous system winds up resulting in more pain which may result in more worry, stress & poor sleep causing more wind-up and then further pain.

When you experience pain anywhere in the body, the sensory centres of the brain then begin to adapt and change resulting in what some experts have called a ‘pain memory’. The more persistent your pain is and the longer you have it, the larger the area affected in the brain. If this process, which has been referred to as central sensitisation, has been occurring for more than 3 months the pain may be referred to as persistent or chronic.


The sympathetic and parasympathetic nervous systems are part of the AUTONOMIC nervous system, which is a branch of the PERIPHERAL NERVOUS SYSTEM. The other branch of the peripheral nervous system is the somatic nervous system. The peripheral nervous system arises out of the central nervous system, which includes the brain and spinal cord.

What is the difference between the autonomic and somatic nervous system since they are both part of the peripheral nervous system? The autonomic system (sympathetic and parasympathetic) controls the involuntary functions of our internal organs and glands. For example, the sympathetic nervous system helps our body deal with stress and is known as the “fight or flight” system. While the parasympathetic balances out our system when the stressor is removed and allows our body to rest. This system is known as the “rest and digest” system.

In contrast, the somatic system controls the voluntary functions of our body. For example, if you touch something hot, your central nervous system processes this information and sends it to your peripheral nervous system, which causes your somatic system to immediately remove your hand from the hot item.

The autonomic system is unique because it has TWO neurons that synapse (come together) in an autonomic ganglion. This is important because each system (sympathetic and parasympathetic) each have preganglionic and postganglionic neurons, which are made up of special fibers (like cholinergic, adrenergic etc.) and this determines what type of neurotransmitters will be released.


Everything you need to know about the vagus nerve

The vagus nerve is the longest and most complex of the 12 pairs of cranial nerves that emanate from the brain. It transmits information to or from the surface of the brain to tissues and organs elsewhere in the body.

The name “vagus” comes from the Latin term for “wandering.” This is because the vagus nerve wanders from the brain into organs in the neck, chest, and abdomen.

It is also known as the 10th cranial nerve or cranial nerve X.

Share on Pinterest The vagus nerve is one of the cranial nerves that connect the brain to the body.

The vagus nerve has two bunches of sensory nerve cell bodies, and it connects the brainstem to the body. It allows the brain to monitor and receive information about several of the body’s different functions.

There are multiple nervous system functions provided by the vagus nerve and its related parts. The vagus nerve functions contribute to the autonomic nervous system, which consists of the parasympathetic and sympathetic parts.

The nerve is responsible for certain sensory activities and motor information for movement within the body.

Essentially, it is part of a circuit that links the neck, heart, lungs, and the abdomen to the brain.

What does the vagus nerve affect?

The vagus nerve has a number of different functions. The four key functions of the vagus nerve are:

  • Sensory: From the throat, heart, lungs, and abdomen.
  • Special sensory: Provides taste sensation behind the tongue.
  • Motor: Provides movement functions for the muscles in the neck responsible for swallowing and speech.
  • Parasympathetic: Responsible for the digestive tract, respiration, and heart rate functioning.

Its functions can be broken down even further into seven categories. One of these is balancing the nervous system.

The nervous system can be divided into two areas: sympathetic and parasympathetic. The sympathetic side increases alertness, energy, blood pressure, heart rate, and breathing rate.

The parasympathetic side, which the vagus nerve is heavily involved in, decreases alertness, blood pressure, and heart rate, and helps with calmness, relaxation, and digestion. As a result, the vagus nerve also helps with defecation, urination, and sexual arousal.

Other vagus nerve effects include:

  • Communication between the brain and the gut: The vagus nerve delivers information from the gut to the brain.
  • Relaxation with deep breathing: The vagus nerve communicates with the diaphragm. With deep breaths, a person feels more relaxed.
  • Decreasing inflammation: The vagus nerve sends an anti-inflammatory signal to other parts of the body.
  • Lowering the heart rate and blood pressure: If the vagus nerve is overactive, it can lead to the heart being unable to pump enough blood around the body. In some cases, excessive vagus nerve activity can cause loss of consciousness and organ damage.
  • Fear management: The vagus nerve sends information from the gut to the brain, which is linked to dealing with stress, anxiety, and fear – hence the saying, “gut feeling.” These signals help a person to recover from stressful and scary situations.

Stimulation of the vagus nerve is a medical procedure that is used to try to treat a variety of conditions. It can be done either manually or through electrical pulses.

The effectiveness of vagus nerve stimulation has been tested through clinical trials. Consequently, the United States Food and Drug Administration (FDA) has approved its use to treat two different conditions.

Epilepsy

In 1997, the FDA allowed the use of vagus nerve stimulation for refractory epilepsy.

This involves a small, electrical device, similar to a pacemaker, being placed in a person’s chest. A thin wire known as a lead runs from the device to the vagus nerve.

The device is placed in the body by surgery under general anesthetic. It then sends electrical impulses at regular intervals, throughout the day, to the brain via the vagus nerve to reduce the severity, or even stop, seizures.

Side effects of vagus nerve stimulation for epilepsy include:

  • hoarseness or changes in voice
  • shortness of breath
  • coughing
  • slow heart rate
  • difficulty swallowing
  • stomach discomfort or nausea

People using this form of treatment should always tell their doctor if they are having any problems as there may be ways to reduce or stop these.

Mental illness

In 2005, the FDA approved the use of vagus nerve stimulation as a treatment for depression. It has also been found to help with the following conditions:


37.3 Regulation of Body Processes

Hormones have a wide range of effects and modulate many different body processes. The key regulatory processes that will be examined here are those affecting the excretory system, the reproductive system, metabolism, blood calcium concentrations, growth, and the stress response.

Hormonal Regulation of the Excretory System

Maintaining a proper water balance in the body is important to avoid dehydration or over-hydration (hyponatremia). The water concentration of the body is monitored by osmoreceptors in the hypothalamus, which detect the concentration of electrolytes in the extracellular fluid. The concentration of electrolytes in the blood rises when there is water loss caused by excessive perspiration, inadequate water intake, or low blood volume due to blood loss. An increase in blood electrolyte levels results in a neuronal signal being sent from the osmoreceptors in hypothalamic nuclei. The pituitary gland has two components: anterior and posterior. The anterior pituitary is composed of glandular cells that secrete protein hormones. The posterior pituitary is an extension of the hypothalamus. It is composed largely of neurons that are continuous with the hypothalamus.

The hypothalamus produces a polypeptide hormone known as antidiuretic hormone (ADH) , which is transported to and released from the posterior pituitary gland. The principal action of ADH is to regulate the amount of water excreted by the kidneys. As ADH (which is also known as vasopressin) causes direct water reabsorption from the kidney tubules, salts and wastes are concentrated in what will eventually be excreted as urine. The hypothalamus controls the mechanisms of ADH secretion, either by regulating blood volume or the concentration of water in the blood. Dehydration or physiological stress can cause an increase of osmolarity above 300 mOsm/L, which in turn, raises ADH secretion and water will be retained, causing an increase in blood pressure. ADH travels in the bloodstream to the kidneys. Once at the kidneys, ADH changes the kidneys to become more permeable to water by temporarily inserting water channels, aquaporins, into the kidney tubules. Water moves out of the kidney tubules through the aquaporins, reducing urine volume. The water is reabsorbed into the capillaries lowering blood osmolarity back toward normal. As blood osmolarity decreases, a negative feedback mechanism reduces osmoreceptor activity in the hypothalamus, and ADH secretion is reduced. ADH release can be reduced by certain substances, including alcohol, which can cause increased urine production and dehydration.

Chronic underproduction of ADH or a mutation in the ADH receptor results in diabetes insipidus . If the posterior pituitary does not release enough ADH, water cannot be retained by the kidneys and is lost as urine. This causes increased thirst, but water taken in is lost again and must be continually consumed. If the condition is not severe, dehydration may not occur, but severe cases can lead to electrolyte imbalances due to dehydration.

Another hormone responsible for maintaining electrolyte concentrations in extracellular fluids is aldosterone , a steroid hormone that is produced by the adrenal cortex. In contrast to ADH, which promotes the reabsorption of water to maintain proper water balance, aldosterone maintains proper water balance by enhancing Na + reabsorption and K + secretion from extracellular fluid of the cells in kidney tubules. Because it is produced in the cortex of the adrenal gland and affects the concentrations of minerals Na + and K + , aldosterone is referred to as a mineralocorticoid , a corticosteroid that affects ion and water balance. Aldosterone release is stimulated by a decrease in blood sodium levels, blood volume, or blood pressure, or an increase in blood potassium levels. It also prevents the loss of Na + from sweat, saliva, and gastric juice. The reabsorption of Na + also results in the osmotic reabsorption of water, which alters blood volume and blood pressure.

Aldosterone production can be stimulated by low blood pressure, which triggers a sequence of chemical release, as illustrated in Figure 37.7. When blood pressure drops, the renin-angiotensin-aldosterone system (RAAS) is activated. Cells in the juxtaglomerular apparatus, which regulates the functions of the nephrons of the kidney, detect this and release renin . Renin, an enzyme, circulates in the blood and reacts with a plasma protein produced by the liver called angiotensinogen. When angiotensinogen is cleaved by renin, it produces angiotensin I, which is then converted into angiotensin II in the lungs. Angiotensin II functions as a hormone and then causes the release of the hormone aldosterone by the adrenal cortex, resulting in increased Na + reabsorption, water retention, and an increase in blood pressure. Angiotensin II in addition to being a potent vasoconstrictor also causes an increase in ADH and increased thirst, both of which help to raise blood pressure.

Hormonal Regulation of the Reproductive System

Regulation of the reproductive system is a process that requires the action of hormones from the pituitary gland, the adrenal cortex, and the gonads. During puberty in both males and females, the hypothalamus produces gonadotropin-releasing hormone (GnRH), which stimulates the production and release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary gland. These hormones regulate the gonads (testes in males and ovaries in females) and therefore are called gonadotropins . In both males and females, FSH stimulates gamete production and LH stimulates production of hormones by the gonads. An increase in gonad hormone levels inhibits GnRH production through a negative feedback loop.

Regulation of the Male Reproductive System

In males, FSH stimulates the maturation of sperm cells. FSH production is inhibited by the hormone inhibin, which is released by the testes. LH stimulates production of the sex hormones ( androgens ) by the interstitial cells of the testes and therefore is also called interstitial cell-stimulating hormone.

The most widely known androgen in males is testosterone. Testosterone promotes the production of sperm and masculine characteristics. The adrenal cortex also produces small amounts of testosterone precursor, although the role of this additional hormone production is not fully understood.

Everyday Connection

The Dangers of Synthetic Hormones

Some athletes attempt to boost their performance by using artificial hormones that enhance muscle performance. Anabolic steroids, a form of the male sex hormone testosterone, are one of the most widely known performance-enhancing drugs. Steroids are used to help build muscle mass. Other hormones that are used to enhance athletic performance include erythropoietin, which triggers the production of red blood cells, and human growth hormone, which can help in building muscle mass. Most performance enhancing drugs are illegal for non-medical purposes. They are also banned by national and international governing bodies including the International Olympic Committee, the U.S. Olympic Committee, the National Collegiate Athletic Association, the Major League Baseball, and the National Football League.

The side effects of synthetic hormones are often significant and non-reversible, and in some cases, fatal. Androgens produce several complications such as liver dysfunctions and liver tumors, prostate gland enlargement, difficulty urinating, premature closure of epiphyseal cartilages, testicular atrophy, infertility, and immune system depression. The physiological strain caused by these substances is often greater than what the body can handle, leading to unpredictable and dangerous effects and linking their use to heart attacks, strokes, and impaired cardiac function.

Regulation of the Female Reproductive System

In females, FSH stimulates development of egg cells, called ova, which develop in structures called follicles. Follicle cells produce the hormone inhibin, which inhibits FSH production. LH also plays a role in the development of ova, induction of ovulation, and stimulation of estradiol and progesterone production by the ovaries, as illustrated in Figure 37.9. Estradiol and progesterone are steroid hormones that prepare the body for pregnancy. Estradiol produces secondary sex characteristics in females, while both estradiol and progesterone regulate the menstrual cycle.

In addition to producing FSH and LH, the anterior portion of the pituitary gland also produces the hormone prolactin (PRL) in females. Prolactin stimulates the production of milk by the mammary glands following childbirth. Prolactin levels are regulated by the hypothalamic hormones prolactin-releasing hormone (PRH) and prolactin-inhibiting hormone (PIH) , which is now known to be dopamine. PRH stimulates the release of prolactin and PIH inhibits it.

The posterior pituitary releases the hormone oxytocin , which stimulates uterine contractions during childbirth. The uterine smooth muscles are not very sensitive to oxytocin until late in pregnancy when the number of oxytocin receptors in the uterus peaks. Stretching of tissues in the uterus and cervix stimulates oxytocin release during childbirth. Contractions increase in intensity as blood levels of oxytocin rise via a positive feedback mechanism until the birth is complete. Oxytocin also stimulates the contraction of myoepithelial cells around the milk-producing mammary glands. As these cells contract, milk is forced from the secretory alveoli into milk ducts and is ejected from the breasts in milk ejection (“let-down”) reflex. Oxytocin release is stimulated by the suckling of an infant, which triggers the synthesis of oxytocin in the hypothalamus and its release into circulation at the posterior pituitary.

Hormonal Regulation of Metabolism

Blood glucose levels vary widely over the course of a day as periods of food consumption alternate with periods of fasting. Insulin and glucagon are the two hormones primarily responsible for maintaining homeostasis of blood glucose levels. Additional regulation is mediated by the thyroid hormones.

Regulation of Blood Glucose Levels by Insulin and Glucagon

Cells of the body require nutrients in order to function, and these nutrients are obtained through feeding. In order to manage nutrient intake, storing excess intake and utilizing reserves when necessary, the body uses hormones to moderate energy stores. Insulin is produced by the beta cells of the pancreas, which are stimulated to release insulin as blood glucose levels rise (for example, after a meal is consumed). Insulin lowers blood glucose levels by enhancing the rate of glucose uptake and utilization by target cells, which use glucose for ATP production. It also stimulates the liver to convert glucose to glycogen, which is then stored by cells for later use. Insulin also increases glucose transport into certain cells, such as muscle cells and the liver. This results from an insulin-mediated increase in the number of glucose transporter proteins in cell membranes, which remove glucose from circulation by facilitated diffusion. As insulin binds to its target cell via insulin receptors and signal transduction, it triggers the cell to incorporate glucose transport proteins into its membrane. This allows glucose to enter the cell, where it can be used as an energy source. However, this does not occur in all cells: some cells, including those in the kidneys and brain, can access glucose without the use of insulin. Insulin also stimulates the conversion of glucose to fat in adipocytes and the synthesis of proteins. These actions mediated by insulin cause blood glucose concentrations to fall, called a hypoglycemic “low sugar” effect, which inhibits further insulin release from beta cells through a negative feedback loop.

This animation describe the role of insulin and the pancreas in diabetes.

Impaired insulin function can lead to a condition called diabetes mellitus , the main symptoms of which are illustrated in Figure 37.10. This can be caused by low levels of insulin production by the beta cells of the pancreas, or by reduced sensitivity of tissue cells to insulin. This prevents glucose from being absorbed by cells, causing high levels of blood glucose, or hyperglycemia (high sugar). High blood glucose levels make it difficult for the kidneys to recover all the glucose from nascent urine, resulting in glucose being lost in urine. High glucose levels also result in less water being reabsorbed by the kidneys, causing high amounts of urine to be produced this may result in dehydration. Over time, high blood glucose levels can cause nerve damage to the eyes and peripheral body tissues, as well as damage to the kidneys and cardiovascular system. Oversecretion of insulin can cause hypoglycemia , low blood glucose levels. This causes insufficient glucose availability to cells, often leading to muscle weakness, and can sometimes cause unconsciousness or death if left untreated.

When blood glucose levels decline below normal levels, for example between meals or when glucose is utilized rapidly during exercise, the hormone glucagon is released from the alpha cells of the pancreas. Glucagon raises blood glucose levels, eliciting what is called a hyperglycemic effect, by stimulating the breakdown of glycogen to glucose in skeletal muscle cells and liver cells in a process called glycogenolysis . Glucose can then be utilized as energy by muscle cells and released into circulation by the liver cells. Glucagon also stimulates absorption of amino acids from the blood by the liver, which then converts them to glucose. This process of glucose synthesis is called gluconeogenesis . Glucagon also stimulates adipose cells to release fatty acids into the blood. These actions mediated by glucagon result in an increase in blood glucose levels to normal homeostatic levels. Rising blood glucose levels inhibit further glucagon release by the pancreas via a negative feedback mechanism. In this way, insulin and glucagon work together to maintain homeostatic glucose levels, as shown in Figure 37.11.

Visual Connection

Pancreatic tumors may cause excess secretion of glucagon. Type I diabetes results from the failure of the pancreas to produce insulin. Which of the following statement about these two conditions is true?

  1. A pancreatic tumor and type I diabetes will have the opposite effects on blood sugar levels.
  2. A pancreatic tumor and type I diabetes will both cause hyperglycemia.
  3. A pancreatic tumor and type I diabetes will both cause hypoglycemia.
  4. Both pancreatic tumors and type I diabetes result in the inability of cells to take up glucose.

Regulation of Blood Glucose Levels by Thyroid Hormones

The basal metabolic rate, which is the amount of calories required by the body at rest, is determined by two hormones produced by the thyroid gland: thyroxine , also known as tetraiodothyronine or T4, and triiodothyronine , also known as T3. These hormones affect nearly every cell in the body except for the adult brain, uterus, testes, blood cells, and spleen. They are transported across the plasma membrane of target cells and bind to receptors on the mitochondria resulting in increased ATP production. In the nucleus, T3 and T4 activate genes involved in energy production and glucose oxidation. This results in increased rates of metabolism and body heat production, which is known as the hormone’s calorigenic effect.

T3 and T4 release from the thyroid gland is stimulated by thyroid-stimulating hormone (TSH) , which is produced by the anterior pituitary. TSH binding at the receptors of the follicle of the thyroid triggers the production of T3 and T4 from a glycoprotein called thyroglobulin . Thyroglobulin is present in the follicles of the thyroid, and is converted into thyroid hormones with the addition of iodine. Iodine is formed from iodide ions that are actively transported into the thyroid follicle from the bloodstream. A peroxidase enzyme then attaches the iodine to the tyrosine amino acid found in thyroglobulin. T3 has three iodine ions attached, while T4 has four iodine ions attached. T3 and T4 are then released into the bloodstream, with T4 being released in much greater amounts than T3. As T3 is more active than T4 and is responsible for most of the effects of thyroid hormones, tissues of the body convert T4 to T3 by the removal of an iodine ion. Most of the released T3 and T4 becomes attached to transport proteins in the bloodstream and is unable to cross the plasma membrane of cells. These protein-bound molecules are only released when blood levels of the unattached hormone begin to decline. In this way, a week’s worth of reserve hormone is maintained in the blood. Increased T3 and T4 levels in the blood inhibit the release of TSH, which results in lower T3 and T4 release from the thyroid.

The follicular cells of the thyroid require iodides (anions of iodine) in order to synthesize T3 and T4. Iodides obtained from the diet are actively transported into follicle cells resulting in a concentration that is approximately 30 times higher than in blood. The typical diet in North America provides more iodine than required due to the addition of iodide to table salt. Inadequate iodine intake, which occurs in many developing countries, results in an inability to synthesize T3 and T4 hormones. The thyroid gland enlarges in a condition called goiter , which is caused by overproduction of TSH without the formation of thyroid hormone. Thyroglobulin is contained in a fluid called colloid, and TSH stimulation results in higher levels of colloid accumulation in the thyroid. In the absence of iodine, this is not converted to thyroid hormone, and colloid begins to accumulate more and more in the thyroid gland, leading to goiter.

Disorders can arise from both the underproduction and overproduction of thyroid hormones. Hypothyroidism , underproduction of the thyroid hormones, can cause a low metabolic rate leading to weight gain, sensitivity to cold, and reduced mental activity, among other symptoms. In children, hypothyroidism can cause cretinism, which can lead to mental retardation and growth defects. Hyperthyroidism , the overproduction of thyroid hormones, can lead to an increased metabolic rate and its effects: weight loss, excess heat production, sweating, and an increased heart rate. Graves’ disease is one example of a hyperthyroid condition.

Hormonal Control of Blood Calcium Levels

Regulation of blood calcium concentrations is important for generation of muscle contractions and nerve impulses, which are electrically stimulated. If calcium levels get too high, membrane permeability to sodium decreases and membranes become less responsive. If calcium levels get too low, membrane permeability to sodium increases and convulsions or muscle spasms can result.

Blood calcium levels are regulated by parathyroid hormone (PTH) , which is produced by the parathyroid glands, as illustrated in Figure 37.12. PTH is released in response to low blood Ca 2+ levels. PTH increases Ca 2+ levels by targeting the skeleton, the kidneys, and the intestine. In the skeleton, PTH stimulates osteoclasts, which causes bone to be reabsorbed, releasing Ca 2+ from bone into the blood. PTH also inhibits osteoblasts, reducing Ca 2+ deposition in bone. In the intestines, PTH increases dietary Ca 2+ absorption, and in the kidneys, PTH stimulates reabsorption of the CA 2+ . While PTH acts directly on the kidneys to increase Ca 2+ reabsorption, its effects on the intestine are indirect. PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the intestines to increase absorption of dietary calcium. PTH release is inhibited by rising blood calcium levels.

Hyperparathyroidism results from an overproduction of parathyroid hormone. This results in excessive calcium being removed from bones and introduced into blood circulation, producing structural weakness of the bones, which can lead to deformation and fractures, plus nervous system impairment due to high blood calcium levels. Hypoparathyroidism, the underproduction of PTH, results in extremely low levels of blood calcium, which causes impaired muscle function and may result in tetany (severe sustained muscle contraction).

The hormone calcitonin , which is produced by the parafollicular or C cells of the thyroid, has the opposite effect on blood calcium levels as does PTH. Calcitonin decreases blood calcium levels by inhibiting osteoclasts, stimulating osteoblasts, and stimulating calcium excretion by the kidneys. This results in calcium being added to the bones to promote structural integrity. Calcitonin is most important in children (when it stimulates bone growth), during pregnancy (when it reduces maternal bone loss), and during prolonged starvation (because it reduces bone mass loss). In healthy nonpregnant, unstarved adults, the role of calcitonin is unclear.

Hormonal Regulation of Growth

Hormonal regulation is required for the growth and replication of most cells in the body. Growth hormone (GH) , produced by the anterior portion of the pituitary gland, accelerates the rate of protein synthesis, particularly in skeletal muscle and bones. Growth hormone has direct and indirect mechanisms of action. The first direct action of GH is stimulation of triglyceride breakdown (lipolysis) and release into the blood by adipocytes. This results in a switch by most tissues from utilizing glucose as an energy source to utilizing fatty acids. This process is called a glucose-sparing effect . In another direct mechanism, GH stimulates glycogen breakdown in the liver the glycogen is then released into the blood as glucose. Blood glucose levels increase as most tissues are utilizing fatty acids instead of glucose for their energy needs. The GH mediated increase in blood glucose levels is called a diabetogenic effect because it is similar to the high blood glucose levels seen in diabetes mellitus.

The indirect mechanism of GH action is mediated by insulin-like growth factors (IGFs) or somatomedins, which are a family of growth-promoting proteins produced by the liver, which stimulates tissue growth. IGFs stimulate the uptake of amino acids from the blood, allowing the formation of new proteins, particularly in skeletal muscle cells, cartilage cells, and other target cells, as shown in Figure 37.13. This is especially important after a meal, when glucose and amino acid concentration levels are high in the blood. GH levels are regulated by two hormones produced by the hypothalamus. GH release is stimulated by growth hormone-releasing hormone (GHRH) and is inhibited by growth hormone-inhibiting hormone (GHIH) , also called somatostatin.

A balanced production of growth hormone is critical for proper development. Underproduction of GH in adults does not appear to cause any abnormalities, but in children it can result in pituitary dwarfism , in which growth is reduced. Pituitary dwarfism is characterized by symmetric body formation. In some cases, individuals are under 30 inches in height. Oversecretion of growth hormone can lead to gigantism in children, causing excessive growth. In some documented cases, individuals can reach heights of over eight feet. In adults, excessive GH can lead to acromegaly , a condition in which there is enlargement of bones in the face, hands, and feet that are still capable of growth.

Hormonal Regulation of Stress

When a threat or danger is perceived, the body responds by releasing hormones that will ready it for the “fight-or-flight” response. The effects of this response are familiar to anyone who has been in a stressful situation: increased heart rate, dry mouth, and hair standing up.

Evolution Connection

Fight-or-Flight Response

Interactions of the endocrine hormones have evolved to ensure the body’s internal environment remains stable. Stressors are stimuli that disrupt homeostasis. The sympathetic division of the vertebrate autonomic nervous system has evolved the fight-or-flight response to counter stress-induced disruptions of homeostasis. In the initial alarm phase, the sympathetic nervous system stimulates an increase in energy levels through increased blood glucose levels. This prepares the body for physical activity that may be required to respond to stress: to either fight for survival or to flee from danger.

However, some stresses, such as illness or injury, can last for a long time. Glycogen reserves, which provide energy in the short-term response to stress, are exhausted after several hours and cannot meet long-term energy needs. If glycogen reserves were the only energy source available, neural functioning could not be maintained once the reserves became depleted due to the nervous system’s high requirement for glucose. In this situation, the body has evolved a response to counter long-term stress through the actions of the glucocorticoids, which ensure that long-term energy requirements can be met. The glucocorticoids mobilize lipid and protein reserves, stimulate gluconeogenesis, conserve glucose for use by neural tissue, and stimulate the conservation of salts and water. The mechanisms to maintain homeostasis that are described here are those observed in the human body. However, the fight-or-flight response exists in some form in all vertebrates.

The sympathetic nervous system regulates the stress response via the hypothalamus. Stressful stimuli cause the hypothalamus to signal the adrenal medulla (which mediates short-term stress responses) via nerve impulses, and the adrenal cortex, which mediates long-term stress responses, via the hormone adrenocorticotropic hormone (ACTH) , which is produced by the anterior pituitary.

Short-term Stress Response

When presented with a stressful situation, the body responds by calling for the release of hormones that provide a burst of energy. The hormones epinephrine (also known as adrenaline) and norepinephrine (also known as noradrenaline) are released by the adrenal medulla. How do these hormones provide a burst of energy? Epinephrine and norepinephrine increase blood glucose levels by stimulating the liver and skeletal muscles to break down glycogen and by stimulating glucose release by liver cells. Additionally, these hormones increase oxygen availability to cells by increasing the heart rate and dilating the bronchioles. The hormones also prioritize body function by increasing blood supply to essential organs such as the heart, brain, and skeletal muscles, while restricting blood flow to organs not in immediate need, such as the skin, digestive system, and kidneys. Epinephrine and norepinephrine are collectively called catecholamines.

Watch this Discovery Channel animation describing the flight-or-flight response.

Long-term Stress Response

Long-term stress response differs from short-term stress response. The body cannot sustain the bursts of energy mediated by epinephrine and norepinephrine for long times. Instead, other hormones come into play. In a long-term stress response, the hypothalamus triggers the release of ACTH from the anterior pituitary gland. The adrenal cortex is stimulated by ACTH to release steroid hormones called corticosteroids . Corticosteroids turn on transcription of certain genes in the nuclei of target cells. They change enzyme concentrations in the cytoplasm and affect cellular metabolism. There are two main corticosteroids: glucocorticoids such as cortisol , and mineralocorticoids such as aldosterone. These hormones target the breakdown of fat into fatty acids in the adipose tissue. The fatty acids are released into the bloodstream for other tissues to use for ATP production. The glucocorticoids primarily affect glucose metabolism by stimulating glucose synthesis. Glucocorticoids also have anti-inflammatory properties through inhibition of the immune system. For example, cortisone is used as an anti-inflammatory medication however, it cannot be used long term as it increases susceptibility to disease due to its immune-suppressing effects.

Mineralocorticoids function to regulate ion and water balance of the body. The hormone aldosterone stimulates the reabsorption of water and sodium ions in the kidney, which results in increased blood pressure and volume.

Hypersecretion of glucocorticoids can cause a condition known as Cushing’s disease , characterized by a shifting of fat storage areas of the body. This can cause the accumulation of adipose tissue in the face and neck, and excessive glucose in the blood. Hyposecretion of the corticosteroids can cause Addison’s disease , which may result in bronzing of the skin, hypoglycemia, and low electrolyte levels in the blood.


Watch the video: Νευρικό Σύστημα Μέρος Στ: Αυτόνομο Νευρικό Σύστημα (July 2022).


Comments:

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