Beta 3-adrenoceptors in the cardiovascular system.

Behind the classic beta 1 and beta 2-adrenoceptors, recent molecular and pharmacological studies have described a new receptor, called the beta 3-adrenoceptor, in various mammalian tissues (brown and white adipose tissue, digestive smooth muscle). Few authors have investigated the putative existence of the beta 3-adrenoceptor in the cardiovascular system. This paper reviews the available data. In vitro studies show that beta 3-adrenoceptor agonists (BRL 37344, CGP 12177) induce a relaxation of fragments of rat carotid artery which is not antagonized by propranolol. In dogs, these drugs elicit a decrease in blood pressure due to peripheral vasodilation and an increase in heart rate which is of baroreflex origin. The vasodilating effects are mainly observed in cutaneous and adipose tissue vessels and cannot be explained by any known transductional mechanism. Activation of this vascular beta 3-adrenoceptor requires higher doses of catecholamines than for beta 1- or beta 2-adrenoceptors. In humans, the cardiovascular effects of beta 3-adrenoceptor agonists are explained by the activation of beta 1- or beta 2 (and not beta 3-)-adrenoceptors. These studies suggest the presence of vascular (but not cardiac) beta 3-adrenoceptors in dogs. In other species, including man, the presence of such cardiac beta 3-adrenoceptors remains to be resolved. Their physiological relevance remains unknown.