Haemodynamic effects of propranolol in hypertension: a review

Like hypertension which is a multifactorial disease, the blood pressure response to propranolol cannot be explained by one mechanism alone to the exclusion of all others. Acute (intravenous) administration of propranolol lowers cardiac output and slows heart rate but does not significantly alter blood pressure. With continued therapy however, blood pressure (in responders) is gradually reduced while cardiac output and rate remains low, indicating a readaptation of total peripheral resistance (TPR) to the new haemodynamic conditions. This relatively complex interplay of factors and the predominant role of TPR in blood pressure response help explain why haemodynamic indices (such as elevated heart rate and cardiac output) were found of little value in predicting response to therapy and the failure of propranolol to control transient pressor responses associated with stress; although the increase of output in response to stress was blocked pressure rose due to increase in TPR. Therefore, despite the obvious cardiac effects of beta-adrenergic blockade, a blood pressure response to propranolol cannot be used as an index of cardiac participation in that hypertension. The long-term changes in TPR were significantly (P less than 0-02) correlated with reduction in plasma renin activity (PRA). This association does not necessarily imply a causal relationship since PRA suppression occurs at lower doses and much more rapidly than alterations in blood pressure. Further, the hypotensive effect obtained by adding propranolol to diuretic therapy was not associated with a significant reduction in PRA. However, the absence of correlation in a group of patients between blood pressure response to propranolol and its effect on other biological variables does not mean that these variables have no role in the hypotensive response. In fact, in some specific conditions the change in one variable might assume particular importance; thus in the markedly hyperkinetic circulation induced by potent vasodilators, reducing cardiac rate and output may play a major role in controlling persistent hypertension.