Influence of β1- Versus β2-Adrenoceptor Blockade on Left Ventricular Function in Humans
- 1 September 1986
- journal article
- research article
- Published by Wolters Kluwer Health in Journal of Cardiovascular Pharmacology
- Vol. 8 (5) , 1086-1091
- https://doi.org/10.1097/00005344-198609000-00030
Abstract
Pharmacological and radio-ligand binding studies have recently indicated the existence of .beta.2-adrenoceptors in the human heart. Their physiological role, however, remains to be elucidated. The present study investigated in 17 normal, young volunteers the effect on resting left ventricular (LV) function of two types of .beta.-blockers; a predominant .beta.1-adrenoceptor antagonist (atenolol, 50 mg once daily) and ICI 118,551 (20 mg t.i.d.), a new, predominant .beta.2-antagonist. LV function was assessed using M-mode echocardiograms and systolic time intervals. Atenolol, ICI 118,551, and placebo were given according to a randomized, double-blind, cross-over protocol. As compared with placebo, both drugs caused a decrease in resting heart rate, but the reduction by ICI 118,551 was less pronounced. Systolic blood pressure was only reduced by atenolol 8 mm Hg on average. Cardiac output was decreased to the same extent following treatment with atenolol (-20%) as after ICI 118,551 (-17%). These decreases in cardiac output were related to the .beta.-blocker-induced bradycardia, since stroke volumes were not affected during either selective .beta.1- or .beta.2-blockade. In addition, all other echocardiographic variables reflecting LV pump function, such as fractional shortening, velocity of diameter change and of displacements, pre-ejection period, and the ratio of PEP/LVET, were not different from placebo. We conclude that in normal young subjects, global LV pump function is not affected by .beta.1- or by .beta.2-blockade, despite the negative chronotropic effect of both drugs. The bradycardia seen during treatment with ICI 118,551 could be secondary to some .beta.1-blockade produced by ICI 118,551; a second possibility is that the slowing of the heart rate is caused by .beta.2-blockade and that the .beta.2-receptors, which are present in the heart, are involved in heart rate regulation.This publication has 10 references indexed in Scilit:
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