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Eur J Pharmacol. 1995 Dec 29;294(2-3):571-6.

Prevention of cyclosporine A-induced renal vasoconstriction by the endothelin receptor antagonist SB 209670.

Author information

1
Department of Renal Pharmacology, SmithKline Beecham Pharmaceuticals, King of Prussia, PA 19406-0939, USA.

Abstract

Administration of endothelin to inactin-anesthetized rats resulted in a significant renal vasoconstriction as evidenced by a reduction in both renal plasma flow and glomerular filtration rate. Infusion of the novel nonpeptide endothelin ETA/ETB receptor antagonist, (+/-)-SB 209670, [(1RS-2SR,3RS)-3-(2-carboxymethoxy-4-methoxy-phenyl)-5 -(prop-1-yloxy)indane-2-carboxylic acid], significantly attenuated the renal vascular effects of endothelin-1. Intravenous administration of cyclosporine A (50 mg/kg) caused a significant reduction in renal plasma flow and glomerular filtration rate and urine flow and a dramatic increase in renal vascular resistance. Concomitant infusion of (+/-)-SB 209670 abolished the cyclosporine A-induced reduction in renal plasma flow and glomerular filtration rate and attenuated the cyclosporine A-induced fluid retention. The data indicate that endothelin is involved in the acute renal effects of cyclosporine A.

PMID:
8750720
DOI:
10.1016/0014-2999(95)00591-9
[Indexed for MEDLINE]

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