Figure 3.

RAAS regulation in polycystic kidney disease. Renal cysts are thought to compress and disrupt the vascular network in the kidney. The kidney would then become ischemic, which would induce renin release from the juxtaglomerular apparatus. The increase in renin secretion could accelerate the conversion of angiotensinogen to angiotensin I, which is converted by angiotensin-converting enzyme (ACE) to angiotensin II. Activation of angiotensin receptor (AT₁) would initiate cascades of physiological responses that would lead to hypertension.