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RESPONSIVENESS TO VASOACTIVE AGENTS OF CEREBRAL AND MESENTERIC ARTERIES ISOLATED FROM CONTROL AND RESERPINE‐TREATED DOGS

1 Pretreatment of dogs for 20 to 24 h before the start of experiments with reserpine (0.5 mg/kg) depleted noradrenaline from cerebral and mesenteric arteries, the diminution being greater in the latter arteries. 2 Contractile responses of helically‐cut strips of cerebral and mesenteric arteries to noradrenaline were unaffected by pretreatment with reserpine. Tyramine‐induced contractions of mesenteric arteries were markedly attenuated by reserpine‐pretreatment, whereas the contraction of cerebral arteries was not influenced. The contractile response of mesenteric arteries to transmural nerve stimulation or nicotine was abolished by reserpine‐pretreatment, but the relaxation induced by nicotine of cerebral arteries contracted with prostaglandin F2α was not affected Pretreatment with reserpine attenuated the contractions of mesenteric arteries induced by angiotensin II, but did not alter the response of cerebral arteries to 5‐hydroxytryptamine. 3 In prostaglandin‐contracted cerebral and mesenteric arterial strips, relaxant effects of acetylcholine, isoprenaline and K+ were not significantly influenced by reserpine‐pretreatment. 4 It appears that tyramine and nicotine do not release noradrenaline from dog cerebral arteries in amounts sufficient to cause significant contractions. Attenuation of the response to angiotensin II by pretreatment with reserpine is not the result of depletion of noradrenaline from the mesenteric arterial wall but may be due to interference with the mechanism specific to actions of angiotensin II.