The role of renin in the antihypertensive action of beta-adrenoreceptor blocking agents.
Since the original reports suggesting that the antihypertensive action of beta-adrenoreceptor blocking drugs is related to their inhibitory action on renin release, much evidence has been put forward both to refute and support this hypothesis. Our studies of the acute and chronic effects of treatment with propranolol in hypertensive patients showed that the antihypertensive action of the drug was of later onset than the initial cardio-depressant and renin-suppressive effects and had little relationship to the pre-treatment levels of treatment-induced changes in plasma renin activity (PRA). When pindolol was substituted for propranolol in these studies PRA rose, but blood pressure control was undisturbed. Again, in animal experiments, although a range of different beta-adrenoreceptor blocking agents induced decreases in both blood pressure and PRA, the hypotensive effects of pindolol was associated with a rise in PRA. Further, PRA proved to be a poor guide to therapeutic effectiveness in the treatment of an unselected population of hypertensive patients with propranolol. It is concluded that the antihypertensive action of beta-adrenoreceptor blocking agents, as a class, is not dependent upon suppression of PRA.
The role of renin in the antihypertensive action of beta-adrenoreceptor blocking agents. Since the original reports suggesting that the antihypertensive action of beta-adrenoreceptor blocking drugs is related to their inhibitory action on renin release, much evidence has been put forward both to refute and support this hypothesis. Our studies of the acute and chronic effects of treatment with propranolol in hypertensive patients showed that the antihypertensive action of the drug was of later onset than the initial cardio-depressant and renin-suppressive effects and had little relationship to the pre-treatment levels of treatment-induced changes in plasma renin activity (PRA). When pindolol was substituted for propranolol in these studies PRA rose, but blood pressure control was undisturbed. Again, in animal experiments, although a range of different beta-adrenoreceptor blocking agents induced decreases in both blood pressure and PRA, the hypotensive effects of pindolol was associated with a rise in PRA. Further, PRA proved to be a poor guide to therapeutic effectiveness in the treatment of an unselected population of hypertensive patients with propranolol. It is concluded that the antihypertensive action of beta-adrenoreceptor blocking agents, as a class, is not dependent upon suppression of PRA.