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

Eur J Pharmacol. 1995 Dec 29;294(2-3):571-6. doi: 10.1016/0014-2999(95)00591-9.

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.

MeSH terms

  • Animals
  • Cyclosporine / toxicity*
  • Endothelin Receptor Antagonists*
  • Immunosuppressive Agents / toxicity*
  • Indans / pharmacology*
  • Kidney / drug effects*
  • Kidney / physiology
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Endothelin / physiology
  • Vasoconstriction / drug effects*

Substances

  • Endothelin Receptor Antagonists
  • Immunosuppressive Agents
  • Indans
  • Receptors, Endothelin
  • 1H-Indene-2-carboxylic acid, 1-(1,3-benzodioxol-5-yl)-3-(2- (carboxymethoxy)-4-methoxyphenyl)-2,3-dihydro-5-propoxy-, (1S,2R,3S)-
  • Cyclosporine