The interaction between angiotensin and sympathetic vasoconstriction in the isolated artery of the rabbit ear.
1. Infusions or injections of angiotensin into the isolated ear artery preparation of the rabbit produced only feeble vasoconstrictions and depressed the sensitivity of the preparation to sympathetic stimulation, tyramine and noradrenaline.2. The anti-sympathetic effect of angiotensin was not prevented or reversed by noradrenaline or cocaine.3. The vasoconstrictor response to angiotensin was usually markedly increased during sympathetic stimulation or other procedures which liberate endogenous noradrenaline (for example, infusion of tyramine), but not when the perfusion pressure was raised by increasing the flow rate or by infusing noradrenaline.4. The vasoconstrictor action of tyramine was also potentiated by sympathetic stimulation.5. The potentiation by sympathetic stimulation of the responses to angiotensin was prevented by reserpine, guanethidine and phentolamine in concentrations which abolished sympathetic vasoconstriction.6. It is suggested that angiotensin facilitates the release of endogenous noradrenaline and owes part of its vasoconstrictor activity to this property.
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001158:Arteries / Q000187:drug effects; D003042:Cocaine / Q000494:pharmacology; D004336:Drug Antagonism; D004357:Drug Synergism; D004431:Ear, External / Q000098:blood supply; D007269:Injections, Intra-Arterial; D009638:Norepinephrine / Q000494:pharmacology; D010477:Perfusion; D011817:Rabbits; D013564:Sympathetic Nervous System / Q000187:drug effects*; D014439:Tyramine / Q000494:pharmacology
D000804:Angiotensin II; D003042:Cocaine; D009638:Norepinephrine; D014439:Tyramine