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Endothelium‐dependent calcium‐induced relaxation in the presence of Ca 2+ ‐antagonists in canine depolarized coronary arteries
Author(s) -
Kikkawa Kohei,
Murata Sakae,
Nagao Taku
Publication year - 1989
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.1476-5381.1989.tb12645.x
Subject(s) - diltiazem , nifedipine , verapamil , calcium , chemistry , endothelium , coronary arteries , mesenteric arteries , vasodilation , artery , medicine , endothelium derived relaxing factor , endocrinology , biophysics , biology
1 We examined the mechanisms underlying Ca 2+ ‐induced relaxation in the presence of clentiazem, a new Ca 2+ ‐antagonist, in depolarized coronary arteries of the dog. 2 Ca 2+ (3 × 10 −5 −3 × 10 −3 m ) caused an unexpected relaxation in the presence of a high concentration of clentiazem (10 −6 m ) in coronary, but not in mesenteric or renal arteries. 3 The Ca 2+ ‐induced relaxation was also observed in the presence of established Ca 2+ ‐antagonists such as diltiazem (3 × 10 −6 m ), nifedipine (3 × 10 −8 m ) and verapamil (3 × 10 −6 m ). 4 The Ca 2+ ‐induced relaxation was inhibited by removal of the endothelium, treatment with oxyhaemoglobin (1.5 × 10 −6 m ) or methylene blue (10 −5 m ), but not by treatment with indomethacin (5 × 10 −6 m ). 5 The Ca 2+ ‐induced relaxation was observed in an endothelium‐denuded coronary artery segment when closely apposed to an endothelium‐containing segment of coronary or mesenteric artery. 6 These results suggest that Ca 2+ ‐induced relaxation in the presence of high concentrations of Ca 2+ ‐antagonists is mediated through endothelium‐derived relaxing factor (EDRF). In addition, Ca 2+ ‐antagonists do not affect the Ca 2+ ‐influx necessary for the release and/or synthesis of EDRF.