Figure FIGURE.

 Illustration of the mechanisms underlying cardiovascular effects of central sympatholytic drugs. Central sympatholytic drugs inhibit central sympathetic discharge via activation of α₂A, α₂C, or imidazoline 1 (I₁) receptors in the brainstem, resulting in decreased heart rate, cardiac output, and total peripheral resistance (TPR). Activation of prejunctional α₂A and α₂C receptors causing inhibition of norepinephrine (NE) release from peripheral sympathetic nerve terminals also contributes to reduction in blood pressure (not shown in the Figure). Activation of α₂B receptors, which are located postjunctionally in the vascular smooth muscle may cause transient vasoconstriction and blood pressure elevation during rapid drug administration.