David's grandfather suffers from hypertension (abnormally high blood pressure). His doctor tells him that part of his problem stems from renal arteriosclerosis (characterized by abnormal thickening and hardening of the walls of the renal arteries, with resulting loss of elasticity). Why would this cause hypertension?
What will be an ideal response?
Renal arteriosclerosis would restrict blood flow to the kidneys and produce renal ischemia. Decreased blood flow and ischemia would together trigger the juxtaglomerular apparatus to produce more renin, which would lead to elevated levels of angiotensin II and aldosterone. Angiotensin II causes vasoconstriction, increased peripheral resistance, and thus increased blood pressure. On the other hand, aldosterone will promote sodium retention. This would lead to more water retained by the body and an increase in blood volume. This too would contribute to a higher blood pressure. Another factor to consider would be the release of more erythropoietin in response to tissue hypoxia. The erythropoietin would stimulate the formation of red blood cells, which would lead to increased blood viscosity and again contribute to the hypertension.
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