Regulation of water excretion

Body water homeostasis is effected by thirst and the urine concentrating and diluting functions of the kidney. These in turn are controlled by intracellular osmoreceptors, principally in the hypothalamus, to some extent by volume receptors in capacitance vessels close to the heart, and via the renin-angiotensin system. Of these, the major and best-understood control is via osmoreceptors. Changes in the plasma Na+ concentration and osmolality are sensed by osmoreceptors that influence both thirst and the release of ADH (also called vasopressin) from the supraoptic and paraventricular nuclei.

ADH plays a central role in urinary concentration by increasing the water permeability of the normally impermeable cortical and medullary collecting ducts. The ability of ADH to increase the urine osmolality is related indirectly to transport in the ascending limb of the loop of Henle, which reabsorbs NaCl without water. This process, which is the primary step in the countercurrent mechanism, has two effects: it makes the tubular fluid dilute and the medullary interstitium concentrated. In the absence of ADH, little water is reabsorbed in the collecting ducts, and a dilute urine is excreted. In contrast, the presence of ADH promotes water reabsorption in the collecting ducts down the favourable osmotic gradient between the tubular fluid and the more concentrated interstitium. As a result, there is an increase in urine osmolality and a decrease in urine volume.

The cortical collecting duct has two cell types with very different functions:

• Principal cells (about 65%) have sodium and potassium channels in the apical membrane and, as in all sodium-reabsorbing cells, Na⁺/K⁺-ATPase pumps in the basolateral membrane.
• Intercalated cells, in comparison, do not transport NaCl (since they have a lower level of Na⁺/K⁺-ATPase activity) but play a role in hydrogen and bicarbonate handling and in potassium reabsorption in states of potassium depletion.

The ADH-induced increase in collecting duct water permeability occurs primarily in the principal cells. ADH acts on V2 (vasopressin) receptors located on the basolateral surface of principal cells, resulting in the activation of adenyl cyclase. This leads to protein kinase activation and to preformed cytoplasmic vesicles that contain unique water channels (called aquaporins) moving to and then being inserted into the luminal membrane. The water channels span the luminal membrane and permit water movement into the cells down a favourable osmotic gradient. This water is then rapidly returned to the systemic circulation across the basolateral membrane. When the ADH effect has worn off, the water channels aggregate within clathrin-coated pits, from which they are removed from the luminal membrane by endocytosis and returned to the cytoplasm. A defect in any step in this pathway, such as in attachment of ADH to its receptor or the function of the water channel, can cause resistance to the action of ADH and an increase in urine output. This disorder is called nephrogenic diabetes insipidus.

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1. [...] that have a higher carbohydrate content and osmolality before you partake in physical exercise. …Health Nova: Your Ultimate Medical Portal Regulation of …Changes in the plasma Na+ concentration and osmolality are sensed by osmoreceptors that influence [...]

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