Evaluation of angiotensins II and III as vasoconstrictors in the hepatic and hindlimb vasculatures of dogs.

Previous work has demonstrated that intravenously administered angiotensin II is more potent than angiotensin III as a systemic vasopressor agent. We tested the hypothesis that this difference in potency is caused at least partially by angiotensin II being more potent than angiotensin III as a vasoconstrictor in the hindlimb and hepatic vasculatures. The effects of angiotensins II and III on hindlimb and hepatic blood flow were evaluated in 14 dogs anesthetized with pentobarbital. Blood flows were measured electromagnetically. Graded doses of angiotensins II and III were administered as bolus injections directly into the arterial supply of the hindlimb and liver. On the basis of duration and graphic integration of the flow responses, but not on the basis of absolute changes in amplitude, angiotensin II was significantly more potent than angiotensin III as a vasoconstrictor in the hindlimb vasculature. In the hepatic circulation the flow changes produced by angiotensin II and angiotensin III were not significantly different on the basis of duration, graphic integration, or amplitude. We conclude that (i) differential vasoconstrictor responses of the hindlimb, but not the hepatic circulation, to angiotensins II and III contribute to the difference in systemic vasopressor potency between these two peptides, and (ii) because flow responses are an integral event with duration and constantly varying amplitude, evaluation of vasoconstrictor potency based only upon amplitude of the flow changes can be misleading.