Role of the Autonomic Nervous System in the Renal Vasoconstriction Response to Hemorrhage in the Rabbit

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Abstract
In normal unanesthetized rabbits with intact autonomic effectors, rapid removal of 26% of the blood volume resulted in prolonged renal vasoconstriction. This response was completely absent in rabbits without functioning autonomic effectors (after guanethidine treatment + adrenalectomy + atropine), despite the greater arterial hypotension in this group. The effects of removing 26% and 32% of the blood volume were compared in the normal innervated and chronically surgically denervated kidney of the same animal. After 26% hemorrhage, the vessels of both kidneys constricted, but the response was significantly greater on the innervated side; reduction in GFR was the same in both kidneys. After 32% hemorrhage the renal constrictor response was greater than after 26% hemorrhage, the difference largely resulting from additional humoral effects, as estimated by the greater vasoconstriction observed in the hypersensitive surgically denervated kidney at this level of hemorrhage; GFR also fell more on the denervated side. The results indicate that sympatho-adrenal activity is essential in the production of renal vasoconstriction after hemorrhage, and suggest that this response is normally produced by the synergistic action of increased sympathetic nerve activity and humoral effects, including those of the adrenal catecholamines.