This review discusses the localization of
adrenergic- and dopaminergic-
adrenoceptors within the cardiovascular system and describes the cardiovascular and renal changes produced following the activation of these receptors by appropriate agonists. Whereas the role of alpha- and beta-
adrenergic agents in the treatment of
heart failure is well recognized, recent studies with
dopamine (DA)-receptor agonists indicate that they offer a novel approach in the
therapy of
congestive heart failure. DA-
adrenoceptor agonists reduce afterload by causing vasodilation and promote
sodium excretion via direct activation of DA1-adrenoceptors located on renal tubules.
Fenoldopam is a selective DA1-adrenoceptor agonist found to be effective in
heart failure. It reduces afterload by causing peripheral vasodilation and produces natriuresis and diuresis.
Dopexamine is a DA1- and beta 2-adrenoceptor agonist, and its efficacy in
heart failure is due to its ability to provide mild inotropic support and cause a reduction in afterload.
Ibopamine is a
prodrug that is converted into its active metabolite,
epinine. This compound activates primarily DA1- and DA2-adrenoceptors. It is effective in
heart failure, and the mechanism progresses via DA1- and DA2-adrenoceptor-mediated reduction in afterload. Agonists of DA2-adrenoceptors reduce afterload by decreasing the release of
norepinephrine and by reducing the levels of renin-angiotensin-aldosterone system. Since both of these systems are active in
heart failure,
ibopamine offers a rational approach for
therapy. The present review addresses the concept of pharmacologic intervention in
adrenergic and dopaminergic influence in the cardiovascular and renal systems to produce changes that are desirable for the
pharmacotherapy of
congestive heart failure.