The influence of circulating catecholamines and prostaglandins on canine renal hemodynamics during hemorrhage.

The relationship between circulating catecholamines and prostaglandins and the independent contribution of circulating catecholamines to renal vasoconstriction during hemorrhage is unknown. The renal hemodynamic effects of a 30% decrease in blood pressure by hemorrhage were therefore studied in three groups of anesthetized dogs which had undergone prior bilateral renal denervation. A constant unilateral infusion of the catecholamine antagonist phenoxybenzamine (POB, 0.2 micrograms/kg per min) into the renal artery during hemorrhage was also performed. In the control (C) dogs (n = 6), hemorrhage was not associated with significant changes in glomerular filtration rate (GFR) or renal blood flow (RBF) in either POB-infused and denervated or noninfused, denervated kidneys. In the second group of dogs (n = 8), pretreated with the prostaglandin inhibitor indomethacin (IN, 10 mg/kg, iv), POB-infused and denervated kidneys had a significantly higher GFR (30 vs. 23 ml/min, P less than 0.05) and RBF (180 vs. 130 ml/min, P less than 0.0-5) than contralateral denervated kidneys during the hemorrhage period. Similar results were observed in the third group of dogs (n = 6) pretreated with the chemically dissimilar prostaglandin inhibitor meclofenemate (M). Circulating plasma catecholamines increased to a similar degree in C (116 to 530 pg/ml, P less than 0.005), IN (116 to 488 pg/ml, P less than 0.005), and M (75 to 315 pg/ml, P less than 0.01) groups; the major part of this increase was due to an increase in plasma norepinephrine (NE). These results indicate that, in this model of hemorrhage, plasma NE exerts a moderate but significant renal vasoconstrictor effect which is unmasked by prostaglandin inhibition.