Regulation of Water Balance

Fluid and electrolyte balance is maintained by autonomic, endocrine, and behavioral means. The renal blood flow is under autonomic control, as is the juxtaglomerular apparatus, which releases renin, an enzyme that acts on angiotensinogen to produce a range of angiotensin hormones. After conversion to angiotensin, this hormone both increases vasoconstriction (thus supporting blood pressure) and aldosterone secretion, as well as causing drinking by direct action on the brain. The drinking behavior appears to be mediated by angiotensin II leaking across the blood-brain barrier in the organum vasculosum at the anterior end of the third ventricle, near preoptic neurons expressing angiotensin II receptors. These neurons then project into the hypothalamus to affect salivary secretion (dry mouth, a signal to drink) and activate general arousal (foraging for water) and specific motor systems (that increase licking and swallowing responses) associated with drinking.

The endocrine response to dehydration has both anterior and posterior pituitary limbs. The release of vasopressin by the posterior pituitary causes active resorption of salt and water in the distal limb of the renal tubules and in the collecting ducts. At the same time, vasopressin has a direct vasoconstrictor effect that supports blood pressure. The anterior pituitary gland releases more ACTH, under control of both corticotropin-releasing hormone and vasopressin secreted into the pituitary portal circulation from the hypothalamus. Cortisol itself has some mineralocorticoid effects, but ACTH also primes the adrenal cortex to make aldosterone, the major mineralocorticoid. Aldosterone secretion is also stimulated by the presence of angiotensin III.

Individuals with lesions in the preoptic area sometimes have inability to appreciate thirst. Some of these individuals also have deficits in vasopressin secretion in response to dehydration. Such patients must be reminded to drink, especially on hot days, to avoid dehydration.

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