Skip to search formSkip to main contentSkip to account menu

BMS 182874

Known as: BMS-182874 
National Institutes of Health

Papers overview

Semantic Scholar uses AI to extract papers important to this topic.
2008
2008
A new rat model for thrombus-induced ischemic pain (TIIP); development of bilateral mechanical allodynia
Highly Cited
2008
Highly Cited
2008
Xanthine oxidase and mitochondria contribute to vascular superoxide anion generation in DOCA-salt hypertensive rats.
Vascular superoxide anion (O(2)(*-)) levels are increased in DOCA-salt hypertensive rats. We hypothesized that the endothelin (ET… 
2005
2005
The endothelin receptor antagonist decreases ischemia/reperfusion-induced tumor necrosis factor production in isolated rat hearts.
Highly Cited
2003
Highly Cited
2003
Cardiac fibrosis occurs early and involves endothelin and AT-1 receptors in hypertension due to endogenous angiotensin II.
2002
2002
Aortic smooth muscle cell phenotypic modulation and fibrillar collagen deposition in angiotensin II-dependent hypertension.
Highly Cited
1995
Highly Cited
1995
Orally Active Endothelin Receptor Antagonist BMS‐182874 Suppresses Neointimal Development in Balloon‐Injured Rat Carotid Arteries
Vascular smooth muscle cell (SMC) proliferation is an important component in the development of restenosis. Because endothelin… 
1995
1995
BMS-182874 is a selective, nonpeptide endothelin ETA receptor antagonist.
BMS-182874 [5-(dimethylamino)-N-(3,4-dimethyl-5-isoxazolyl)-1-naphthalene sulfonamide] is a recently discovered, low molecular… 
Highly Cited
1995
Highly Cited
1995
Selective blockade of the endothelin subtype A receptor decreases early atherosclerosis in hamsters fed cholesterol.
Recent studies suggest that endothelin and its receptors may be involved in atherogenesis. To test this hypothesis, cholesterol… 
1995
1995
Aspartate mutation distinguishes ETA but not ETB receptor subtype‐selective ligand binding while abolishing phospholipase C activation in both receptors
Highly Cited
1994
Highly Cited
1994
Mutation of peptide binding site in transmembrane region of a G protein-coupled receptor accounts for endothelin receptor subtype selectivity.
By clicking accept or continuing to use the site, you agree to the terms outlined in our Privacy Policy (opens in a new tab), Terms of Service (opens in a new tab), and Dataset License (opens in a new tab)