Role of catecholamine and adenosine in the ischemic response following release of a renal artery occlusion.

The mechanism responsible for the postocclusive vasoconstriction of the renal artery of dog was analyzed by pharmacological evaluation.The renal circulation responded variably animal by animal after the release of occlusion.Among 36 nontreated dogs, the vasoconstriction, i. e., “reactive ischemia”, the vasodilation, i. e., “reactive hyperemia”, and no change in the vascular response, i. e., “dumb response” were obtained after 1 minute occlusion in 53, 33 and 14 per cent respectively. The number of the reactive ischemia among 9 reserpinized animals diminished to 33 per cent, while the number of the reactive hyperemia and dumb response increased to 44 and 23 per cent respectively.The reactive ischemia was blocked completely by phenoxybenzamine (α-adrenergic blocking agent) treatment, while this phenomenon was potentiated remarkably by the treatment of dipyridamole (adenosine deaminase inhibitor). Dipyridamole treatment potentiated also vasoconstrictory response of adenosine, AMP and noradrenaline.In cases of absence of the postocclusive vasoconstriction, noradrenaline or adenosine infusion or successive infusions of both substances converted the vascular response to the reactive ischemia, while AMP or angiotensin infusion did not modify the postocclusive vascular response at all.These results imply that catecholamine-adenosine system would play a dominant role in the mechanism of the postocclusive vasoconstriction of the renal artery.