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Vasodilation, not cardiodepression, underlies the antihypertensive effect of beta-adrenoceptor antagonists.

Most antihypertensive drugs act by counteracting vasoconstrictor mechanisms and lower blood pressure by lowering vascular resistance. The beta blockers, which have the unique ability to counteract cardiac sympathetic drive, seem to be a major exception to this. Moreover, their degree of cardiodepression is directly correlated with the initial sympathetic tone and also with their degree of intrinsic sympathomimetic activity (ISA). Cardiodepression initially evokes a baroreflex-mediated proportional rise in vascular resistance. As indicated by review of the literature, the antihypertensive effect of beta blockers always parallels a decline in vascular resistance. Studying beta blockers with different degrees of ISA in 50 hypertensive patients after minimizing cardiac sympathetic drive by strict bed rest showed that the initial effect of the drug is offset by a rise in vascular resistance proportional to the fall in cardiac output. After that, blood pressure always fell in parallel with vascular resistance, whatever the absolute level of cardiac output. In the long run, blood pressure and vascular resistance were always positively correlated, irrespective of the level of cardiac output. Thus, like all other antihypertensive agents, beta blockers also lower blood pressure through interference with a vasoconstrictor mechanism.