BIOLOGY Volume 3 - A Textbook of General Biology - 2004

20. EXCRETION AND OSMOREGULATION

20.6. Osmoregulation, Antidiuretic Hormone, and the Production of Concentrated or Dilute Urine

A relatively stable Osmotic Pressure of the Blood is maintained through a balance between Water intake (from food and drink) and water loss (via exhaled air, sweat, feces, and urine), as shown in Fig. 20.9. However, the fine-tuning of osmotic pressure is primarily the responsibility of the antidiuretic hormone (ADH). The production of large volumes of dilute urine is referred to as diuresis, whereas the opposite phenomenon is called antidiuresis. The antidiuretic effect of ADH consists in reducing the volume of urine produced and, consequently, increasing the concentration of solutes within it. ADH is a peptide (Table 17.10); it is also sometimes called vasopressin.

This hormone is produced by the Hypothalamus and transported from there to the posterior Pituitary Gland via neurosecretion, as discussed in Section 17.6.2.

In cases of insufficient water intake, heavy sweating, or the consumption of a high-salt meal, highly sensitive osmoreceptors in the hypothalamus detect an increase in the osmotic pressure of the blood. Nerve impulses are generated and transmitted to the posterior pituitary, triggering the release of ADH. Carried by the bloodstream to the Kidneys, the hormone increases the water permeability of the distal convoluted tubules and collecting ducts. This is achieved by increasing the number of water channels in their Cell membranes. Analogous to Ion Channels, these water channels are transport Proteins. They are synthesized within The Cell, stored in the membranes of small Golgi vesicles, and accumulated in the Cytoplasm. Upon binding to specific cell-surface receptors, ADH—acting via cAMP (the second messenger system described in Sections 17.6.1 and 17.6.2)—stimulates the fusion of these vesicles with The Plasma Membrane. When ADH secretion ceases, the process is reversed: the vesicles containing the transport proteins are internalized via endocytosis and stored within the cell until the next "command" is issued by ADH.

The increase in the number of water channels leads to an enhanced osmotic outflow of water from the nephron lumen into the tissue fluid of the renal cortex and medulla, thereby reducing urine volume and making it more concentrated (Fig. 20.26). The water is subsequently carried away by the bloodstream.

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Fig. 20.26. Diagram illustrating The Effect of antidiuretic hormone (ADH) on the water permeability of the Distal convoluted tubule and collecting duct.

ADH also increases the permeability of the collecting duct to urea, which diffuses from the urine into the medullary tissue fluid. As a result, medullary osmolarity increases, which further enhances the outflow of water from the thin descending limb of the Loop of Henle.

Conversely, after drinking a large amount of water, the osmotic pressure of the blood drops and ADH secretion stops. The walls of the distal convoluted tubule and collecting duct become impermeable to water, water reabsorption during the filtrate's passage through the medulla decreases, and, as a result, a large volume of hypotonic urine is excreted (Fig. 20.26).

Table 20.5 summarizes the processes involved in water balance regulation, and Fig. 20.27 provides an overall scheme of the interactions regulating water and salt balance. The hypothalamus also houses the "thirst center." When blood osmolarity is very high (osmotic potential is strongly negative), this center stimulates the urge to drink.

A deficiency of ADH leads to a condition known as diabetes insipidus, characterized by The excretion of very large quantities of hypotonic urine. The fluid loss via urine must be compensated for by copious fluid intake.

Table 20.5. Changes induced by antidiuretic hormone (ADH) in the epithelium of the distal convoluted tubule and collecting duct

Fig. 20.27. General scheme for The regulation of plasma osmotic potential.