The Role of Central and Peripheral α- and ß-Adrenoceptors in the Control of Cardiovascular Function

Abstract

Central α₂-Adrenoceptor. α₂-Adrenoceptors exist postsynaptically on dendrites of neurons in the nucleus tracus solitarii (NTS), which is the first synapse in the central component of the cardiovascular reflex loop. Inhibitory neurons from the NTS course to the vasomotor center (VMC), while excitatory neurons from the NTS traverse to the dorsal motor nucleus of the vagus (DMNV). Stimulation of α₂-adrenoceptors in the NTS by central α₂-adrenoceptor agonists, such as Clonidine, results in the activation of the inhibitory neurons to the VMC, causing sympathetic outflow to the peripheral vasculature, heart, and kidney to be reduced. Consequently, peripheral vascular resistance, heart rate, and renin release are decreased resulting in a reduction in blood pressure. In addition, stimulation of central α₂-adrenoceptors results in the activation of the excitatory neurons to the DMNV, which causes enhanced cholinergic outflow to the heart, producing yet a further decrease in heart rate and cardiac output [1].