Beta-receptor-mediated increase in venous return in humans.

To assess the involvement of beta 1- and beta 2-receptors in the regulation of venous return in humans, changes in left ventricular end-diastolic (LVED) dimension were determined during beta-receptor stimulation either by exogenous catecholamines or by increased endogenous sympathetic activity after hydralazine, after placebo and during nonselective versus beta 1-selective blockade. Taking changes in heart rate and LV emptying into account, the three beta-agonists (isoproterenol, terbutaline, and epinephrine) as well as hydralazine increased venous return as inferred from LVED dimension. After hydralazine, nonselective and beta 1-selective blockade were equally effective in blunting the increases in venous return, in heart rate, and in positive inotropic response. Beta 1-Selective blockade did not affect the increase in heart rate caused by epinephrine and partially inhibited the positive inotropic effect and the increase in venous return. Nonselective blockade not only blocked the increase in venous return owing to epinephrine but actually led to a decrease, as evidenced by a decrease in LVED dimension despite the marked bradycardia and high afterload with this combination. The present findings in healthy humans indicate that stimulation of both beta 1- and beta 2-receptors increases venous return, heart rate, and myocardial contractility. Beta 1-Receptors appear to predominate in the response to neuronal sympathetic activity.