Higher Level Of Venous Return Increased Antidiuretic Hormone
Regulation of blood osmolarity
Regulation of blood pressure
Regulation of blood osmolarity
Regulation of blood pressure
In the kidney: ADH increases permeability of collecting duct cells and distal tubule cells to H2O
In the kidney: ADH increases permeability of collecting duct cells and distal tubule cells to H2O
51.14 Antidiuretic Hormone Increases Blood Pressure and Promotes Water Resorption ADH is produced by neurons in the hypothalamus and released from their axons in the posterior pituitary. The release of ADH is stimulated by hypothalamic osmoreceptors and inhibited by stretch receptors in the great arteries.
ADH controls the permeability of the collecting ducts by stimulating the production and activity of membrane proteins that form water channels. These proteins, called aquaporins, are found in many tissues that are permeable to water—for example, the capillary endothelium, red blood cells, and the proximal convoluted tubules of the kidney. Differences among tissues in water permeability can be related to the presence or absence of aquaporins. Aquaporins are expressed in the descending limb of the loop of Henle, for example, but not in the ascending limb. One particular aquaporin that is found in distal convoluted tubule and collecting duct cells is controlled by ADH on both a long-term and a short-term basis. Over the long term, ADH levels influence the expression of the gene for this aquaporin; over the short term, ADH controls the insertion of the aquaporin into the cells' plasma membranes.
ADH also helps regulate blood osmolarity by controlling water resorption. Sensory cells in the hypothalamus monitor the osmolarity of the blood. If blood osmolarity increases, these osmoreceptors stimulate increased release of ADH to enhance water resorption from the kidneys. The osmoreceptors also stimulate thirst. The resulting water retention and water intake dilutes the blood as it expands blood volume.
Blood pressure and osmolarity are regulated by ADH
When you lose blood volume, your blood pressure tends to fall. Besides activating the kidney autoregulatory mechanisms described in the previous section, a drop in blood pressure decreases the activity of the stretch receptors in the walls of the aorta and the carotid arteries (see Figure 49.17). These stretch receptors provide information to cells in the hypothalamus that produce antidiuretic hormone (ADH, also called vasopressin) and send it down their axons to the posterior pituitary gland. As stretch receptor activity decreases, the production and release of this hormone increases (Figure 51.14).
ADH acts on the distal convoluted tubules and collecting ducts of the kidney to increase their permeability to water. When the circulating level of ADH is high, the distal tubules and the collecting ducts are very permeable to water, more water is resorbed from the urine, and only small quantities of concentrated urine are produced, thus conserving blood volume and maintaining blood pressure. When ADH levels are low, water is not resorbed from the collecting ducts, and lots of dilute urine is produced.
The heart produces a hormone that influences kidney function
When systemic venous return to the heart increases and the atria of the heart become more stretched, the atrial muscle fibers release a peptide hormone called atrial natriuretic pep-tide (ANP). This peptide hormone enters the circulation, and when it reaches the kidney, it decreases the resorption of sodium. The result is an increased loss of sodium and water, which has the effect of lowering blood volume and blood pressure. In pathological situations in which a weakened heart cannot pump enough blood to keep up with the venous return (congestive heart failure), the atria become stretched more than normal, and the resulting high levels of ANP in the blood can be a useful diagnostic measure.
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