Home | | Medical Physiology | Physiological Functions of ADH

Chapter: Medical Physiology: Pituitary Hormones and Their Control by the Hypothalamus

| Study Material, Lecturing Notes, Assignment, Reference, Wiki description explanation, brief detail |

Physiological Functions of ADH

The injection of extremely minute quantities of ADH—as small as 2 nanograms—can cause decreased excretion of water by the kidneys (antidiuresis).

Chemical Structures of ADH and Oxytocin

Both oxytocin and ADH (vasopressin) are polypep-tides, each containing nine amino acids. Their amino acid sequences are the following:

Vasopressin: Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-GlyNH2

Oxytocin: Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-GlyNH2 Note that these two hormones are almost identical except that in vasopressin, phenylalanine and arginine replace isoleucine and leucine of the oxytocin molecule. The similarity of the molecules explains their partial functional similarities.

Physiological Functions of ADH

The injection of extremely minute quantities of ADH—as small as 2 nanograms—can cause decreased excretion of water by the kidneys (antidiuresis). Briefly, in the absence of ADH, the collecting tubules and ducts become almost impermeable to water, which prevents significant reabsorption of water and there-fore allows extreme loss of water into the urine, also causing extreme dilution of the urine. Conversely, in the presence of ADH, the permeability of the collect-ing ducts and tubules to water increases greatly and allows most of the water to be reabsorbed as the tubular fluid passes through these ducts, thereby con-serving water in the body and producing very concen-trated urine.

The precise mechanism by which ADH acts on the collecting ducts to increase their permeability is only partially known. Without ADH, the luminal mem-branes of the tubular epithelial cells of the collecting ducts are almost impermeable to water. However, immediately inside the cell membrane are a large number of special vesicles that have highly water-permeable pores called aquaporins. When ADH acts on the cell, it first combines with membrane receptors that activate adenylyl cyclase and cause the formation of cAMP inside the tubular cell cytoplasm. This causes phosphorylation of elements in the special vesicles, which then causes the vesicles to insert into the apical cell membranes, thus providing many areas of high water permeability. All this occurs within 5 to 10 minutes. Then, in the absence of ADH, the entire process reverses in another 5 to 10 minutes. Thus, this process temporarily provides many new pores that allow free diffusion of water from the tubular fluid through the tubular epithelial cells and into the renal interstitial fluid. Water is then absorbed from the col-lecting tubules and ducts by osmosis, in relation to the urine-concentrating mechanism of the kidneys.

Regulation of ADH Production Osmotic Regulation. When a concentrated electrolytesolution is injected into the artery that supplies the hypothalamus, the ADH neurons in the supraoptic and paraventricular nuclei immediately transmit impulses into the posterior pituitary to release large quantities of ADH into the circulating blood, sometimes increas-ing the ADH secretion to as high as 20 times normal. Conversely, injection of a dilute solution into this artery causes cessation of the impulses and therefore almost total cessation of ADH secretion.Thus, the con-centration of ADH in the body fluids can change from small amounts to large amounts, or vice versa, in only a few minutes.

The precise way that the osmotic concentration of the extracellular fluid controls ADH secretion is not clear. Yet somewhere in or near the hypothalamus are modified neuron receptors called osmoreceptors. When the extracellular fluid becomes too concen-trated, fluid is pulled by osmosis out of the osmore-ceptor cell, decreasing its size and initiating appropriate nerve signals in the hypothalamus to cause additional ADH secretion. Conversely, when the extracellular fluid becomes too dilute, water moves by osmosis in the opposite direction, into the cell, and this decreases the signal for ADH secretion. Although some researchers place these osmoreceptors in the hypothalamus itself (possibly even in the supraoptic nuclei), others believe that they are located in the organum vasculosum, a highly vascular structure in theanteroventral wall of the third ventricle.

Regardless of the mechanism, concentrated body fluids stimulate the supraoptic nuclei, whereas dilute body fluids inhibit them. A feedback control system is available to control the total osmotic pressure of the body fluids.

Vasoconstrictor and Pressor Effects of ADH, and Increased ADH Secretion Caused by Low Blood Volume

Whereas minute concentrations of ADH cause increased water conservation by the kidneys, higher concentrations of ADH have a potent effect of con-stricting the arterioles throughout the body and there-fore increasing the arterial pressure. For this reason, ADH has another name, vasopressin.

One of the stimuli for causing intense ADH secre-tion is decreased blood volume. This occurs especially strongly when the blood volume decreases 15 to 25 per cent or more; the secretory rate then sometimes rises to as high as 50 times normal. The cause of this is the following.

The atria have stretch receptors that are excited by overfilling.When excited, they send signals to the brain to inhibit ADH secretion. Conversely, when the recep-tors are unexcited as a result of underfilling, the oppo-site occurs, with greatly increased ADH secretion. Decreased stretch of the baroreceptors of the carotid, aortic, and pulmonary regions also stimulates ADH secretion. For further details about this blood volume-pressure feedback mechanism.

Study Material, Lecturing Notes, Assignment, Reference, Wiki description explanation, brief detail


Copyright © 2018-2020 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.