The glomerular filtration rate is closely autoregulated over a fairly large range of normal blood pressures. Only at very low blood volumes (low blood pressures) does it decrease to reduce the volume of urine produced. Water reabsorption in the proximal convoluted tubule and loop of Henle is relatively constant. Urine volume is primarily regulated by water reabsorption in the distal tubules and collecting ducts.
Two hormones are critical to the regulation of urine volume. Without these hormones, large amounts of dilute urine are produced. Concentrated urine is produced in the presence of ADH (anti-diuretic hormone; also called vasopressin) and aldosterone. These hormones reduce urine volume to conserve body water.
Reduced blood volume increases the osmolarity of the blood. This causes ADH release from the posterior pituitary. Normally, the distal nephrons are not permeable to water. ADH inserts aquaporins (water channels) into the distal nephrons to allow water reabsorption.
Secretion of aldosterone is controlled by a sequence of reactions that begin at the juxtaglomerular complex, a group of specialized cells at junction of the distal convoluted tubule and loop of Henle, near the glomerular arterioles. Macula densa cells release renin that leads to production of angiotensin II (renin-angiotensin system). Angiotensin II causes vasoconstriction and secretion of aldosterone from the adrenal cortex. Aldosterone increases NaCl reabsorption in the DCT. In the presence of ADH water follows the Na and is reabsorbed to reduce urine volume.
Atrial natriuretic peptide (ANP) is produced by the atria when they are stretched by increased blood volume (blood pressure), such as in congestive heart failure. It is a diuretic: it increases urine volume by increasing GFR and decreasing Na ion reabsorption.
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