Volume-Sensing Mechanisms

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OpenStax Anatomy and Physiology

The body cannot directly measure blood volume, but blood pressure can be measured. Blood pressure often reflects blood volume and is measured by baroreceptors in the aorta and carotid sinuses. When blood pressure increases, baroreceptors send more frequent action potentials to the central nervous system, leading to widespread vasodilation. Included in this vasodilation are the afferent arterioles supplying the glomerulus, resulting in increased GFR, and water loss by the kidneys. If pressure decreases, fewer action potentials travel to the central nervous system, resulting in more sympathetic stimulationproducing vasoconstriction, which will result in decreased filtration and GFR, and water loss.

Decreased blood pressure is also sensed by the granular cells in the afferent arteriole of the JGA. In response, the enzyme renin is released. You saw earlier in the chapter that renin activity leads to an almost immediate rise in blood pressure as activated angiotensin II produces vasoconstriction. The rise in pressure is sustained by the aldosterone effects initiated by angiotensin II; this includes an increase in Na+ retention and water volume. As an aside, late in the menstrual cycle, progesterone has a modest influence on water retention. Due to its structural similarity to aldosterone, progesterone binds to the aldosterone receptor in the collecting duct of the kidney, causing the same, albeit weaker, effect on Na+ and water retention.

Cardiomyocytes of the atria also respond to greater stretch (as blood pressure rises) by secreting ANH. ANH opposes the action of aldosterone by inhibiting the recovery of Na+ by the DCT and collecting ducts. More Na+ is lost, and as water follows, total blood volume and pressure decline. In low-pressure states, ANH does not seem to have much effect.

ADH is also called vasopressin. Early researchers found that in cases of unusually high secretion of ADH, the hormone caused vasoconstriction (vasopressor activity, hence the name). Only later were its antidiuretic properties identified. Synthetic ADH is still used occasionally to stem life-threatening esophagus bleeding in alcoholics.

When blood volume drops 5–10 percent, causing a decrease in blood pressure, there is a rapid and significant increase in ADH release from the posterior pituitary. Immediate vasoconstriction to increase blood pressure is the result. ADH also causes activation of aquaporin channels in the collecting ducts to affect the recovery of water to help restore vascular volume. Diureti

Source:

Betts, J. G., Young, K. A., Wise, J. A., Johnson, E., Poe, B., Kruse, D. H., … DeSaix, P. (n.d.). Anatomy and Physiology. Houston, Texas: OpenStax. Access for free at: https://openstax.org/details/books/anatomy-and-physiology


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