Captopril reduces renal excretion of prostaglandin E2 in the sodium-depleted rabbit |
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| Authors: | A A Attallah |
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| Affiliation: | 1. Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA, USA;2. Departments of Neuroscience and Anesthesia and Pain Management and Peter O’Donnell Brain Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA;3. Spatial Genomics, Inc., Pasadena, CA, USA;4. Departments of Biochemistry and Genome Sciences, University of Washington School of Medicine, Seattle, WA 98195, USA;1. Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, 116044, China;2. School of Life Science and Biotechnology, Dalian University of Technology, Dalian, 116023, China |
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| Abstract: | The effects of captopril on renal function and prostaglandin E2 excretion were investigated in rabbits undergoing chronic sodium depletion. Captopril administered for six days, via rate-controlled osmotic pumps, caused diuresis and marked natriuresis which were accompanied by a significant reduction of urinary prostaglandin E2 excretion and of glomerular filtration rate. It is concluded that captopril reduces the renal excretion of prostaglandin E2 and that its diuretic and natriuretic effects are prostaglandin E2-independent. |
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