Trial reportBritish journal of clinical pharmacology2005
Vasodilator effects of the endothelin ET receptor selective antagonist BMS-193884 in healthy men.
Trial report in British journal of clinical pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Intra-Target Microdosing (ITM): A Novel Drug Development Approach Aimed at Enabling Safer and Earlier Translation of Biological Insights Into Human Testing.Clinical and translational science · 2017Review
- Renal hyperfiltration related to diabetes mellitus and obesity in human disease.World journal of diabetes · 2012Article
- Prolonged pharmacodynamic effects of S-0139, an intravenously administered endothelin A (ET) antagonist, in the human forearm blood flow model.British journal of clinical pharmacology · 2010Article
- Endothelin-1 and hypertension: from bench to bedside.Current hypertension reports · 2008Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
aimsA number of endothelin receptor antagonists (ERAs) are currently in clinical development as potential therapies in states characterized by vasoconstriction, such as systemic hypertension. We investigated the haemodynamic effects of locally and systemically active doses of BMS-193884, an endothelin A (ET(A)) receptor selective ERA, and its influence on vasoconstriction to endothelin-1 (ET-1) in healthy men.
methodsIn three separate randomized, placebo-controlled studies, the forearm blood flow (FBF) response to intra-arterial (i.a.) infusion of ET-1 (5 pmol min(-1)) was assessed during i.a. co-infusion of BMS-193884 (5 and 50 nmol min(-1)), and at 12 and at 24 h after oral administration of BMS-193884 (50, 100 and 200 mg at 12 h; and 200 mg at 24 h). Data were examined by repeated-measures analysis of variance (anova) with treatment and subject as factors.
resultsET-1 caused significant forearm vasoconstriction, attenuated after oral dosing with BMS-193884 (200 mg) at 12 (P < 0.01) and 24 h (P < 0.0001). BMS-193884 (50 nmol min(-1), i.a.) caused local vasodilatation (25 +/- 11%) when infused alone (P = 0.02) and abolished forearm vasoconstriction to ET-1 (P < 0.0001 vs. ET-1 alone). Orally, BMS-193884 (200 mg) caused a reduction in total systemic vascular resistance at 12 (-14 +/- 9%, P = 0.03) and 24 h (-12 +/- 7%, P < 0.0001). There was no rise in plasma ET-1 levels.
conclusionBMS-193884 causes local and systemic vasodilatation and attenuation of local vasoconstriction to ET-1. The absence of a rise in plasma endothelin levels suggests BMS-193884 is selective for the ET(A) receptor. This form of pharmacodynamic modelling may be useful in the development of ERAs in cardiovascular disease.
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