Final answer:
The renin-angiotensin-aldosterone system is activated when the kidneys sense decreased blood flow, leading to the secretion of renin, and the subsequent formation of angiotensin II, which increases blood pressure by causing vasoconstriction, sodium retention, and water retention.
Step-by-step explanation:
Renin-Angiotensin-Aldosterone System
Renal artery stenosis can lead to high blood pressure due to the activation of the renin-angiotensin-aldosterone system (RAAS). When the kidneys detect decreased blood flow, they respond by secreting renin, a crucial enzyme in the RAAS. Renin converts angiotensinogen, a protein made by the liver, into angiotensin I. The angiotensin-converting enzyme (ACE) then converts angiotensin I to angiotensin II, a potent vasoconstrictor that increases blood pressure.
Angiotensin II has several important effects, including stimulating the secretion of aldosterone from the adrenal cortex and promoting sodium retention in the kidneys. These actions collectively increase blood volume and pressure. Additionally, angiotensin II triggers the release of anti-diuretic hormone (ADH), which leads to water retention, further contributing to increased blood pressure. This system plays a direct role in determining blood pressure and volume, with implications for the treatment of hypertension through the use of ACE inhibitors which block the conversion of angiotensin I to angiotensin II, thereby lowering blood pressure.