Effects of alpha-adrenoceptor agonists on cardiac output and blood pressure in spinally anesthetized ganglion-blocked dogs.

The alpha-adrenoceptor agonist ST-1059 (2-amino-1-(2,5-dimethoxyphenyl) ethanol), the alpha 1-adrenoceptor agonist methoxamine, the alpha 2-adrenoceptor agonist clonidine and a nonselective alpha-adrenoceptor agonist norepinephrine, all increase cardiac output and dose-dependently increase arterial blood pressure in spinally anesthetized ganglion-blocked dogs. The increase in cardiac output may be the result of an increased venous return via the contraction of capacitance vessels, and the vasopressor responses are attributed to an increase in total peripheral resistance. The increases in cardiac output and pressor responses induced by ST-1059 and methoxamine were antagonized by the alpha 1-adrenoceptor antagonist prazosin (0.3 mg/kg i.v.), but those induced by clonidine were not inhibited. In contrast, the alpha 2-adrenoceptor antagonist yohimbine (0.3 mg/kg i.v.) had little or no effects on the increase in cardiac output or the pressor responses induced by ST-1059 and methoxamine, but strongly attenuated those of clonidine. Prazosin and yohimbine inhibited the norepinephrine-induced increase in cardiac output and pressor responses. These results suggest that the increases in cardiac output and blood pressure induced by ST-1059 were mediated by postjunctional alpha 1-adrenoceptor stimulation, such as by methoxamine, but that those induced by clonidine were mediated by postjunctional alpha 2-adrenoceptor stimulation in dogs. Not only the postjunctional alpha 1-adrenoceptors but also the postjunctional alpha 2-adrenoceptors may play an important role in the constriction of venous beds, as well as of the arterioles in spinally anesthetized ganglion-blocked dogs.