Figure 1 shows the basic components of the osmoreceptor-ADH feedback system for control of extra cellular fluid sodium concentration and osmolarity. When osmolarity (plasma sodium concentration) increases above normal because of water deficit, for example, this feedback system operates as follows:

1. An increase in extracellular fluid osmolarity (which in practical terms means an increase in plasma sodium concentration) causes the special nerve cells called osmoreceptor cells, located in the anterior hypothalamus near the supraoptic nuclei, to shrink.

2. Shrinkage of the osmoreceptor cells causes them to f ire, sending nerve signals to additional nerve cells in the supraoptic nuclei, which then relay these signals down the stalk of the pituitary gland to the posterior pituitary.

3. These action potentials conducted to the posterior pituitary stimulate the release of ADH, which is stored in secretory granules (or vesicles) in the nerve endings.

 4. ADH enters the blood stream and is transported to the kidneys, where it increases the water permeability of the late distal tubules, cortical collecting tubules, and medullary collecting ducts.

 5. The increased water permeability in the distal nephron segments causes increased water reabsorption and excretion of a small volume of concentrated urine.

Fig1. Osmoreceptor-antidiuretic hormone (ADH) feedback  mechanism for regulating extracellular fluid osmolarity in response  to a water deficit. 

Thus, water is conserved in the body while sodium and other solutes continue to be excreted in the urine. This causes dilution of the solutes in the extracellular fluid, thereby correcting the initial excessively concentrated extracellular fluid.

The opposite sequence of events occurs when the extracellular fluid becomes too dilute (hypoosmotic). For example, with excess water ingestion and a decrease in extracellular fluid osmolarity, less ADH is formed, the renal tubules decrease their permeability for water, less water is reabsorbed, and a large volume of dilute urine is formed. This in turn concentrates the body fluids and returns plasma osmolarity toward normal.

ADH SYNTHESIS IN SUPRAOPTIC AND PARAVENTRICULAR NUCLEI OF THE HYPOTHALAMUS AND ADH RELEASE FROM THE POSTERIOR PITUITARY

Figure 2 shows the neuroanatomy of the hypothalamus and the pituitary gland, where ADH is synthesized and released. The hypothalamus contains two types of magnocellular (large) neurons that synthesize ADH in the supraoptic and paraventricular nuclei of the hypothalamus, about five sixths in the supraoptic nuclei and about one sixth in the paraventricular nuclei. Both of these nuclei have axonal extensions to the posterior pituitary. Once ADH is synthesized, it is transported down the axons of the neurons to their tips, terminating in the posterior pituitary gland. When the supraoptic and para ventricular nuclei are stimulated by increased osmolarity or other factors, nerve impulses pass down these nerve endings, changing their membrane permeability and increasing calcium entry. ADH stored in the secretory granules (also called vesicles) of the nerve endings is released in response to increased calcium entry. The released ADH is then carried away in the capillary blood of the posterior pituitary into the systemic circulation.

Fig2.  Neuroanatomy of the hypothalamus, where antidiuretic hormone (ADH) is synthesized, and the posterior pituitary  gland, where ADH is released.

Secretion of ADH in response to an osmotic stimulus is rapid, so plasma ADH levels can increase severalfold within minutes, thereby providing a rapid means for altering renal excretion of water. 

A second neuronal area important in controlling osmolarity and ADH secretion is located along the anteroventral region of the third ventricle, called the AV3V region. At the upper part of this region is a structure called the subfornical organ, and at the inferior part is another structure called the organum vasculosum of the lamina terminalis. Between these two organs is the median pre optic nucleus, which has multiple nerve connections with the two organs, as well as with the supraoptic nuclei and the blood pressure control centers in the medulla of the brain. Lesions of the AV3V region cause multiple deficits in the control of ADH secretion, thirst, sodium appetite, and blood pressure. Electrical stimulation of this region or stimulation by angiotensin II can increase ADH secretion, thirst, and sodium appetite.

In the vicinity of the AV3V region and the supraoptic nuclei are neuronal cells that are excited by small increases in extracellular fluid osmolarity; hence, the term osmoreceptors has been used to describe these neurons. These cells send nerve signals to the supraoptic nuclei to control their firing and secretion of ADH. It is also likely that they induce thirst in response to increased extracellular fluid osmolarity.

Both the subfornical organ and the organum vasculosum of the lamina terminalis have vascular supplies that lack the typical bloodbrain barrier that impedes the diffusion of most ions from the blood into the brain tissue. This characteristic makes it possible for ions and other solutes to cross between the blood and the local interstitial fluid in this region. As a result, the osmoreceptors rapidly respond to changes in osmolarity of the extracellular fluid, exerting powerful control over the secretion of ADH and over thirst, as discussed later.

STIMULATION OF ADH RELEASE BY DECREASED ARTERIAL PRESSURE AND/OR DECREASED BLOOD VOLUME

ADH release is also controlled by cardiovascular reflexes that respond to decreases in blood pressure and/or blood volume, including (1) the arterial baroreceptor reflexes and (2) the cardiopulmonary reflexes, both of which are discussed in Chapter 18. These reflex pathways originate in high-pressure regions of the circulation, such as the aortic arch and carotid sinus, and in the low-pressure regions, especially in the cardiac atria. Afferent stimuli are carried by the vagus and glossopharyngeal nerves with synapses in the nuclei of the tractus solitarius. Projections from these nuclei relay signals to the hypothalamic nuclei that control ADH synthesis and secretion.

T hus, in addition to increased osmolarity, two other stimuli increase ADH secretion: (1) decreased arterial pressure and (2) decreased blood volume. Whenever blood pressure and blood volume are reduced, such as occurs during hemorrhage, increased ADH secretion causes increased fluid reabsorption by the kidneys, helping to restore blood pressure and blood volume toward normal.

QUANTITATIVE IMPORTANCE OF OSMOLARITY AND CARDIOVASCULAR REFLEXES IN STIMULATING ADH SECRETION

As shown in Figure 3, either a decrease in effective blood volume or an increase in extracellular fluid osmolarity stimulates ADH secretion. However, ADH is considerably more sensitive to small changes in osmolarity than to similar percentage changes in blood volume. For example, a change in plasma osmolarity of only 1 percent is sufficient to increase ADH levels. By contrast, after blood loss, plasma ADH levels do not change appreciably until blood volume is reduced by about 10 percent. With further decreases in blood volume, ADH levels rapidly increase. Thus, with severe decreases in blood volume, the cardiovascular reflexes play a major role in stimulating ADH secretion. The usual day today regulation of ADH secretion during simple dehydration is effected mainly by changes in plasma osmolarity. Decreased blood volume, however, greatly enhances the ADH response to increased osmolarity.

Fig3. The effect of increased plasma osmolarity or decreased  blood volume on the level of plasma (P) antidiuretic hormone (ADH),  also called arginine vasopressin (AVP). (Modified from Dunn FL, Brennan TJ, Nelson AE, et al: The role of blood osmolality and volume in regulating vasopressin secretion in the rat. J Clin Invest 52[12]:3212, 1973. By permission of the American Society of Clinical Investigation.)

OTHER STIMULI FOR ADH SECRETION

ADH secretion can also be increased or decreased by other stimuli to the central nervous system, as well as by various drugs and hormones, as shown in Table1. For example, nausea is a potent stimulus for ADH release, which may increase to as much as 100 times normal after vomiting. Also, drugs such as nicotine and morphine stimulate ADH release, whereas some drugs, such as alcohol, inhibit ADH release. The marked diuresis that occurs after ingestion of alcohol is due in part to inhibition of ADH release.

Table1. Control of ADH Secretion

اخر الاخبار

اخبار العتبة العباسية المقدسة

شركة براق القمّة تعرض نماذج صناعتها من الشاحنات في مهرجان عين الحياة الرابع

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مجموعة مشاتل الكفيل تعرض تشكيلة متكاملة من النباتات الظلية والموسمية في مهرجان عين الحياة الرابع

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المزيد

الآخبار الصحية

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طريقة جديدة لتجديد خلايا الدماغ

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مواضيع ذات صلة

Urine Specific Gravity

Renal Mechanisms for Excreting Dilute Urine

Physiological Control of Glomerular Filtration and Renal Blood Flow

Renal Blood Flow

Determinants of The GFR

Glomerular Filtration—The First Step in Urine Formation

Urine Formation Results From Glomerular Filtration, Tubular Reabsorption, and Tubular Secretion

Multiple Functions of The Kidneys

التنظيم الحمضي – القاعدي في الجسم Acid-Base Balance

حصى الكلية Urinary Caliculi

أمراض الجهاز البولي

آلية التبول