Body water losses are rapidly reflected in blood. Volume and electrolyte changes in response to decreased blood water content (increased osmolal-ity) trigger the hypothalamus to stimulate antidiure-tic hormone (ADH) release from the posterior lobe of the pituitary gland. ADH acts on the kidney to increase tubular water resorption and maintain plasma volume. Decreased plasma volume also
ADH: water resorption Kidneys
Figure 3 Water and sodium physiology: mechanisms controlling body water gain and loss. As water is lost from the body via sweat, urine, respiration, and feces, (1) plasma osmolality increases and plasma volume decreases with water loss. (2) The increase in osmolality acts on the 'thirst center' in the hypothalamus to secrete ADH and stimulates the conscious desire for water. (3) The release of ADH from the pituitary gland increases tubular resorption of water by the kidney. (4) Aldosterone is formed via a series of reactions involving renin, which is released from the adrenal cortex in response to decreased blood pressure, and a plasma protein, angiotensin-gen. Aldosterone promotes sodium resorption by the kidney to maintain plasma volume. (5) These events conserve water and result in the production of concentrated urine.
results in a complex series of events resulting in the release of renin from the kidneys and the subsequent formation of angiotensin II and the minerocorticoid, aldosterone. Angiotensin II is a potent vasoconstrictor and stimulator of thirst. Aldosterone promotes sodium resorption, which allows the blood to retain more water. The net result of these regulatory mechanisms is concentrated urine and maintenance of plasma volume, provided that exogenous fluid intake increases proportionally. If fluid intake is not increased, dehydration will still result.
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