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Research Article Free access | 10.1172/JCI108988

The Role of Renal Nerves and Prostaglandins in Control of Renal Hemodynamics and Plasma Renin Activity during Hypotensive Hemorrhage in the Dog

William L. Henrich, Robert J. Anderson, Arnold S. Berns, Keith M. McDonald, Penny J. Paulsen, Tomas Berl, and Robert W. Schrier

Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80262

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Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80262

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Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80262

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Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80262

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Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80262

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Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80262

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Department of Medicine, University of Colorado Medical Center, Denver, Colorado 80262

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Published March 1, 1978 - More info

Published in Volume 61, Issue 3 on March 1, 1978
J Clin Invest. 1978;61(3):744–750. https://doi.org/10.1172/JCI108988.
© 1978 The American Society for Clinical Investigation
Published March 1, 1978 - Version history
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Abstract

The effects of hypotensive hemorrhage (HH) on renal hemodynamics and plasma renin activity (PRA) during prostaglandin (PG) synthesis inhibition were examined in three groups of dogs. In each group of animals arterial blood pressure was lowered by a 30% decrement. In the first group of eight control animals, HH was not associated with a significant change in glomerular filtration rate (GFR, 42-36 ml/min, NS); renal blood flow (RBF) declined significantly, from 234 to 171 ml/min, P < 0.05. In the second group of eight animals, pretreated with RO 20-5720 (RO, 2 mg/kg), a competitive inhibitor of PG synthesis, HH was associated with a significant fall in GFR (43-17 ml/min, P < 0.001) and RBF (195-89 ml/min, P < 0.001). In the third group of eight animals, pretreatment with indomethacin (IN, 10 mg/kg), a chemically dissimilar PG inhibitor, HH was also associated with a significant fall in GFR (38-8 ml/min, P < 0.001) and RBF (150-30 ml/min, P < 0.001). Renal denervation attenuated this renal ischemic effect of HH in the presence of PG inhibition. In the RO group, GFR (34 vs. 17 ml/min, P < 0.005) and RBF (145 vs. 89 ml/min, P < 0.025) were significantly greater in denervated vs. innervated kidneys during HH. Similarly, in animals treated with IN, a significantly higher GFR (28 vs. 8 ml/min, P < 0.005) and RBF (101 vs. 30 ml/min, P < 0.005) occurred in denervated as compared to innervated kidneys during HH. With HH, the increase in PRA in the control group (3.34-11.68 ng/ml per h, P < 0.005) was no different than that observed in the RO group (4.96-18.9 ng/ml per h, P < 0.001) or IN group (4.71-17.8 ng/ml per h, P < 0.001). In summary, the present results indicate that renal PG significantly attenuate the effect of HH to decrease GFR and RBF. Furthermore, renal denervation exerts a protective effect against the enhanced renal ischemic effects which occur in the presence of PG inhibition during HH. Finally, PG inhibition does not alter the effect of HH to cause an increase in PRA.

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