Mechanisms of antihypertensive action of beta-adrenergic blocking drugs: evidence against potentiation of baroreflexes.

A possibility that can be advanced to explain the antihypertensive effect of beta-blocking drugs is that they act through the baroreflex control of the cardiovascular system. In 38 essential hypertensive patients we measured 1) The lengthening and shortening in R-R interval caused by stimulation or deactivation of arterial baroreceptors (vasoactive drug technique); 2) The fall and rise in blood pressure caused by stimulation and deactivation of carotid baroreceptors (neck chamber); 3) The rise in forearm vascular resistance caused by deactivation of cardiopulmonary receptors (lower body suction). The study was made before and after 6-10 days' administration of nadolol (80-360 mg once a day) or acebutolol (200-600 mg t.i.d.). Nadolol and acebutolol similarly reduced blood pressure and heart rate. Either drug increased heart rate responses to arterial baroreceptor manipulation but the increase fell short of statistical significance. Blood pressure and vasomotor responses to carotid baroreceptor and cardiopulmonary receptor manipulation were also not significantly modified by beta blockade. The baroreceptor control of heart rate and blood pressure showed a modification, however, insofar as a resetting towards the lower blood pressure values occurred. These findings demonstrate that arterial baroreceptor and cardiopulmonary receptor control of circulation is not potentiated by beta-blocking drugs, and that therefore this mechanism cannot account for their antihypertensive effect. The resetting of the baroreflex that occurs during beta blockade may, however, contribute to maintain the hypotension obtained.