Autor: |
Bird JE; Department of Pharmacology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, N.J. 08543, USA., Webb ML, Wasserman AJ, Liu EC, Giancarli MR, Durham SK |
Jazyk: |
angličtina |
Zdroj: |
Pharmacology [Pharmacology] 1995 Jan; Vol. 50 (1), pp. 9-23. |
DOI: |
10.1159/000139262 |
Abstrakt: |
Infusion (0.46 mumol/kg/min) of the endothelin (ET)-converting-enzyme inhibitor, phosphoramidon (P), protected function and structure after 30 min renal ischemia in rats more than treatment (5 mumol/kg/min) with the ETA receptor antagonist, BMS-182874 (B). The glomerular filtration rate (GFR; 0.7 +/- 0.12 ml/min) and renal plasma flow (RPF) decreased approximately 40% at 2 h reflow versus controls (C: 1.2 +/- 0.12). B weakly protected the GFR (0.8 +/- 0.07 ml/min); P restored it (1.1 +/- 0.05). Both compounds reduced tubular injury at 2 h reflow; P ameliorated glomerular changes. At 24 h the GFR (0.6 +/- 0.06 ml/min) and RPF decreased 67% versus C (1.8 +/- 0.08). B did not protect the GFR and RPF. P partially protected the GFR (0.9 +/- 0.07 ml/min) but not RPF, and reduced tubular injury. The results suggest that both ETA and non-ETA receptors mediate ET-induced changes in ischemic renal failure. |
Databáze: |
MEDLINE |
Externí odkaz: |
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