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 μg/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 < 0.05) and RBF (180 vs 130 ml/min, P < 0.05) 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<0.005), IN (116 to 488 pg/ml, P<0.005), and M (75 to 315 pg/ml, P<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.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine