The role of cardiac beta-1 receptors in the hemodynamic response to a beta-2 agonist.
The role of beta 1-receptors in the hemodynamic response to beta 2-stimulation was assessed in seven healthy subjects by infusion of the selective beta 2-agonist terbutaline both with and without selective beta 1-blockade by atenolol (50 mg). Infusion of terbutaline increased heart rate (+28 bpm) and indices of left ventricular (LV) performance associated with a marked decrease in LV end-systolic wall stress. The LV end-diastolic dimension remained unchanged despite the tachycardia, suggesting that venous return had increased. Systolic blood pressure increased, whereas total peripheral resistance and diastolic blood pressure decreased. Atenolol pretreatment caused the hemodynamic changes expected of beta 1-blockade but did not blunt the effects of terbutaline on heart rate, peripheral resistance, or venous return. Increases after terbutaline in LV performance and systolic blood pressure were significantly blunted by atenolol. Stimulation of beta 1-receptors therefore appears to play no role in the chronotropic and only a moderate role in the inotropic response after infusion of a beta 2-agonist. Alternative mechanisms for the cardiac changes with terbutaline include (1) withdrawal of vagal tone, (2) decrease in afterload, and (3) stimulation of cardiac beta 2-receptors.
D000328:Adult; D001262:Atenolol / Q000494:pharmacology*; D004347:Drug Interactions; D004562:Electrocardiography; D004837:Epinephrine / Q000097:blood; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D008297:Male; D009638:Norepinephrine / Q000097:blood; D011943:Receptors, Adrenergic, beta / Q000187:drug effects*; D013726:Terbutaline / Q000494:pharmacology*
D011943:Receptors, Adrenergic, beta; D001262:Atenolol; D013726:Terbutaline; D009638:Norepinephrine; D004837:Epinephrine