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Angiotensin converting enzyme (ACE) inhibitors have the potential to falsely elevate plasma renin activity (PRA). Therefore, in a patient treated with an ACE-inhibitor, the findings of a detectable PRA level or a low serum aldosterone PRA ratio do not exclude the diagnosis of primary aldosteronism. In addition, a strong predictor for primary aldosteronism is a PRA level undetectably low in a patient taking an ACE-inhibitor.
The renal juxtaglomerular apparatus generates renin, an enzyme that converts angiotensinogen to angiotensin I. The inactive angiotensin I is enzymatically converted to the active octapeptide angiotensin II, a potent vasopressor responsible for hypertension of renal origin. Angiotensin II also stimulates the zona glomerulosa of the adrenal cortex to release aldosterone.
Renin secretion by the kidney is stimulated by a fall in glomerular blood pressure, by decreased sodium concentration at the macula densa at the distal tubule, or by stimulation of sympathetic outflow to the kidney, such as in renal vascular diseases.