The hemodynamic profiles of methoxamine and B-HT 933 during a stepwise-increased infusion in spinalized ganglion-blocked dogs show that both compounds induce a dose-dependent increase in arterial blood pressure due to an increase in total peripheral resistance. Methoxamine initially also increases cardiac output, which contributes to the increase in blood pressure. The increased cardiac output is the result of an increased stroke volume, because heart rate is unchanged. B-HT 933 increases neither cardiac output nor heart rate. Because neither compound stimulates the heart directly, the increase in stroke volume induced by methoxamine can be due only to an increased venous return. B-HT 933 appears to be devoid of an effect on the capacitance vessels, because stroke volume and cardiac output are unchanged. The present study suggests that under in vivo conditions, postjunctional alpha 2-adrenoceptors in the capacitance vessels of the dog are not functional.
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