Abstract

α 2 -Adrenergic receptors (α 2 ARs) are essential components of the neural circuitry regulating cardiovascular function. The role of specific α 2 AR subtypes (α 2a , α 2b , and α 2c ) was characterized with hemodynamic measurements obtained from strains of genetically engineered mice deficient in either α 2b or α 2c receptors. Stimulation of α 2b receptors in vascular smooth muscle produced hypertension and counteracted the clinically beneficial hypotensive effect of stimulating α 2a receptors in the central nervous system. There were no hemodynamic effects produced by disruption of the α 2c subtype. These results provide evidence for the clinical efficacy of more subtype-selective α 2 AR drugs.