The mechanisms of antihypertensive action of beta-adrenergic receptor blocking drugs.
Beta-adrenergic receptor blockers lower blood pressure in hypertensive patients and spontaneously hypertensive rats (SHR). The fall in blood pressure is associated with a complex chain of hemodynamic events. The transient effects differ from long-term changes. After reviewing the dynamics of beta-blocker induced hemodynamic changes, we propose a scheme to explain both short-term and long-term effects. In this scheme it is suggested that the primary effects are (1) a fall in cardiac output through blockade of cardiac beta-adrenergic receptors and (2) a promotion of renal tubular sodium and water loss by blockade of renal tubular beta-adrenergic receptors. The initial reactions of the cardiovascular control system to these effects as well as the final adaptations are discussed. It is suggested that for future developments in the field of beta-adrenergic control of blood pressure further analysis of the renal tubular sympathetic control of sodium and water excretion is necessary.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D002302:Cardiac Output / Q000187:drug effects; D006801:Humans; D007668:Kidney / Q000187:drug effects; D011311:Pressoreceptors / Q000187:drug effects; D012018:Reflex / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects
D000319:Adrenergic beta-Antagonists; D000959:Antihypertensive Agents