[Effect of dopamine on perfusion pressure in rat peripheral blood vessels]

Rat mesenteric and hind limb arteries were perfused with the rat's own blood under constant perfusion rate, in situ. The effect of dopamine (DA) administered intraarterially was investigated and compared with effects of norepinephrine (NE), tyramine (Tyr), and phenylephrine (PHE). The magnitude of the vasoconstrictive maximum response of both vasculatures to NE and PHE was larger than those to DA and Tyr, and those to DA were larger than those to Tyr in hind limb, but those to Tyr were more potent than those to DA in the mesenteric artery. The vasoconstriction evoked by celiac ganglionic stimulation was much the same to that evoked by NE and PHE. Under cocaine infusion, the rise in perfusion pressure of both vasculatures evoked by NE and PHE. Under cocaine infusion, the rise in perfusion pressure of both vasculatures evoked by NE was slight, but the duration was markedly potentiated. However, the effect of Tyr was suppressed and that of DA was not changed. In rats on alpha-methyl-rho-tyrosine, the responses of both vasculatures to Tyr were reduced and those to NE and DA were not changed. In the reserpinized rat, the effect of NE was not changed and that of Tyr was reduced, while that of D was more evident in both vasculatures. After phenoxybenzamine treatment, vasoconstrictive effect of DA was reversed in mesenteric and reduced in hind limb artery. Vasodilating effect of DA after phenoxybenzamine, was not changed by treatment with propranolol, atropine, and diphenhydramine but was reduced with reserpine and abolished with haloperidol. These results suggest that the vasoconstrictive effect of DA depends partly on indirect sympathomimetic action, and after phenoxybenzamine, DA acts by vasodilating the DA receptor. Potentiation with reserpine may depend on a post-synaptic mechanism and increase in dopamine-beta-hydroxylase activity.