The possible importance of aldosterone as well as renin in the long-term antihypertensive action of propranolol

Abstract

In 50 patients with essential hypertension, propranolol produced a significant decrease in blood pressure. The decrease in mean pressure was greatest in patients classified by a renin sodium nomogram as having high renin hypertension. In turn, blood pressure decreased more in patients with normal renin than in those with low renin levels. Indeed, a net increase in diastolic pressure occurred in the low renin subgroup. These findings confirm the value of pretreatment plasma renin measurements for predicting blood pressure responses to propranolol. Over-all, seven of the 50 patients exhibited increases in mean blood pressure during propranolol treatment. Presumably, this occurred because the minimal suppression of renin-angiotensinmediated vasoconstriction in these patients was insufficient to compensate for the unopposed alpha-sympathetic vasoconstriction unmasked by peripheral vascular beta-blockade. Within this group of patients, there was a significant inverse correlation between control renin values and the amplitude of the pressor response. The decrements in plasma renin were slightly greater in patients classified as responders (decrease in mean blood pressure ≥ 10 per cent) than in nonresponders. However, when the propranolol-induced decrements in aldosterone excretion were taken into account, responders to treatment exhibited far greater decreases than non-responders. Thus, higher levels of aldosterone during treatment may operate to oppose the antihypertensive action of propranolol. Ultimately, this dependency of the blood pressure response upon aldosterone levels is at least partly coordinated with propranolol-induced inhibition of renin release, since we found a significant correlation between changes in these hormones during treatment.