Renal pharmacology of GR138950, a novel non-peptide angiotensin AT1 receptor antagonist

European Journal of Pharmacology
K L ClarkG M Drew


This paper describes the renal pharmacology of the novel, specific, non-peptide angiotensin AT1 receptor antagonist, GR138950 (1-[[3-bromo-2-[2-[[(trifluoromethyl) sulphonyl] amino] phenyl]-5-benzofuranyl] methyl]-4-cyclopropyl-2-ethyl-1H-imidazole-5- carboxamide). When administered to anaesthetised salt-replete dogs, GR138950 caused renal vasodilatation and significant increases in sodium and urine excretion. No change in glomerular filtration rate was observed indicating that the natriuresis was a consequence of inhibition of tubular sodium reabsorption. Qualitatively similar but less marked changes in renal function were observed in response to the angiotensin converting enzyme inhibitor, captopril, although in contrast to GR138950, captopril also caused a small but significant fall in mean blood pressure. Intra-renal artery infusion of exogenous angiotensin II resulted in dose-related renal vasoconstriction and decreases in urine excretion, sodium excretion, fractional excretion of sodium and glomerular filtration rate. These renal effects of angiotensin II were all markedly antagonised by GR138950. We conclude that GR138950 is an effective antagonist of the renal haemodynamic and excretory actions of endogenous and exogeno...Continue Reading


Sep 1, 1978·European Journal of Pharmacology·R R VollmerV S Murthy
Jan 17, 1977·Pflügers Archiv : European journal of physiology·P J Harris, J A Young
Sep 24, 1991·European Journal of Pharmacology·P C WongP B Timmermans
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Oct 1, 1990·The Journal of Clinical Investigation·M G SeikalyF D Seney
Feb 1, 1989·Journal of Cardiovascular Pharmacology·M SchmidtJ L Imbs

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