![]() |
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Departments of Pharmacology and Medicine, Schools of Medicine, University of Pennsylvania, and the Edward B. Robinette Foundation, Medical Clinic, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
In the chloralose anesthetized dog, renal blood flows were measured (rotameters) simultaneously from acutely denervated and innervated kidneys. Graded hemorrhages of 10, 20 and 30 ml/kg demonstrated an increasingly greater increase in renal vascular resistance in the innervated kidney. Prior administration of guanethidine eliminated the differential changes in renal vascular resistances of the denervated and innervated kidneys. Adrenalectomy did not alter the observed changes. A continued reduction below control values of renal blood flows and an associated pressor response frequently followed rapid restoration of the blood volume to normal. This pressor effect, which was augmented by guanethidine and terminated by phentolamine, was not observed in adrenalectomized animals. It is concluded that the changes in renal vascular resistance during hemorrhage were determined largely by augmented sympathetic nervous activity. A posthemorrhagic pressor response which occurred in 14 of 38 dogs was due to catecholamines from the adrenal medulla.
Accepted on April 27, 1964