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.