The combination of a beta blocker and a vasodilator is logical in the treatment of high blood pressure. Systemic arteriolar dilatation is beneficial to reduce the elevated peripheral resistance and hence to decrease cardiac afterload. β-Adrenoceptor blockade exerts its own antihypertensive activity and also suppresses the reflex tachycardia induced by vasodilatation. The combined β- and α-adrenoceptor blockade exerted by carvedilol imposes these beneficial hemodynamic effects. Carvedilol is a nonselective β-adrenoceptor antagonist, devoid of intrinsic sympathomimetic activity and possessing selective α<sub>1</sub>-adrenoceptor-blocking activity, although this is considerably weaker than its β-adrenoceptor antagonistic activity. One iso-mer [S(-)-carvedilol] contains both the β- and α-adrenoceptor activity, whereas R(+)-carvedilol is only a weak alpha blocker. Carvedilol is produced as the racemate. The hemodynamic profile is in accordance with that to be expected from the combination of beta and alpha blockade.
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