Normal and Altered Function of the Renin-Angiotensin-Aldosterone System in Man

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Abstract
Evidence exists that release of renin is controlled either by stretch sensors in the juxtaglomerular cells of the afferent glomerular arterioles or by Na load sensors in the cells of the macula densa of the distal tubules. "Decreased stretch" and decreased Na load normally go together to increase release of renin which leads, through the production of angiotensin II, to increased secretion of aldosterone. This is characteristic of states of arterial hypovolemia. Arterial hypervolemia induces the opposite sequence, namely, decreased renin and the decreased aldosterone production. However, when the hypervolemia (or the increased distal tubular Na load) is the result of an aldosterone-producing adrenal tumor (primary aldosteronism) the suppression of renin release is accompanied by overproduction of aldosterone since the tumor is autonomous. This unique distortion of the renin-aldosterone system is specifically diagnostic of an aldosterone producing tumor. It has recently been shown that this specific combination also occurs in hypertensive patients without hypokalemia ("essential" hypertension) and that such people can be cured by surgical removal of what, heretofore, have been called "incidental, non-functioning adrenal cortical adenomas," but which are really aldosterone-producing tumors. This situation is estimated to be present in 20% of patients with "essential" hypertension.