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Mechanisms of U46619‐induced contraction of rat pulmonary arteries in the presence and absence of the endothelium
Author(s) -
McKenzie C,
MacDonald A,
Shaw AM
Publication year - 2009
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.2008.00084.x
Subject(s) - niflumic acid , myograph , dids , chemistry , channel blocker , vasoconstriction , pharmacology , carbachol , chloride channel , thromboxane a2 , calcium channel , voltage dependent calcium channel , contraction (grammar) , endocrinology , calcium , medicine , biochemistry , receptor , membrane , organic chemistry
Thromboxane A(2) and endothelial dysfunction are implicated in the development of pulmonary hypertension. The receptor-transduction pathway for U46619 (9,11-dideoxy-9 alpha, 11 alpha-methanoepoxy prostaglandin F(2 alpha))-induced contraction was examined in endothelium-intact (E+) and denuded (E-) rat pulmonary artery rings.