Renin Suppression in Primary Aldosteronism

When Conn and his associates¹ began using plasma renin estimations to differentiate between primary aldosteronism and that secondary to renovascular or malignant hypertension, they provided sound physiological and clinical support for the validity of the test. The renin-angiotensin system is known to stimulate aldosterone secretion and to be in turn inhibited by the latter. Clearly, renin suppression would be expected in primary aldosteronism, but not in malignant or renal vascular hypertension in which excessive renin production, responsible for the high aldosterone level, offsets its restraining effect. Studies on three patients with primary aldosteronism disclosed absence of renin activity, even after provocation by recumbency and low-sodium diet—measures which ordinarily stimulate renin secretion by lowering circulating blood volume. In contrast, three patients with secondary aldosteronism manifested high-renin concentration, whereas three normotensive subjects did not deviate from the normal. Plasma renin estimation appeared destined to become an important diagnostic test.

The need