CARDIOVASCULAR REGULATION IN MICE LACKING ALPHA(2)-ADRENERGIC RECEPTOR SUBTYPE-B AND SUBTYPE-C

alpha(2)-Adrenergic receptors (alpha(2)ARs) are essential components o f the neural circuitry regulating cardiovascular function. The role of specific alpha(2)AR subtypes alpha(2a), alpha(2b), and alpha(2c) was characterized with hemodynamic measurements obtained from strains of g enetically engineered mice deficient in either alpha(2b) or alpha(2c) receptors. Stimulation of alpha(2b) receptors in vascular smooth muscl e produced hypertension and counteracted the clinically beneficial hyp otensive effect of stimulating alpha(2a) receptors in the central nerv ous system. There were no hemodynamic effects produced by disruption o f the alpha(2c) subtype. These results provide evidence for the clinic al efficacy of more subtype-selective alpha(2)AR drugs.