title: Possible involvement of endothelial leukotrienes in acetylcholine-induced contraction in rabbit coronary artery.
abstract: In endothelium-intact preparations of rabbit coronary artery, acetylcholine (3 x 10(-8)-10(-6) M) caused a contraction in the presence of N omega-nitro-L-arginine methyl ester (10(-4) M). Removal of endothelium significantly attenuated the contraction. The present experiments were undertaken to elucidate whether the acetylcholine-induced contraction in endothelium-intact preparations was due to arachidonic acid metabolites, endothelin or superoxide. The acetylcholine-induced contraction in endothelium-intact preparations was attenuated by manoalide (10(-6) M and 3 x 10(-6) M) or oleyloxyethyl phosphorylcholine (10(-5) M) (phospholipase A2 inhibitors), BAY x 1005 (3 x 10(-6) and 10(-5) M) or L 663,536 (10(-6) and 10(-5) M) (leukotriene synthesis inhibitors) and ONO-1078 (10(-6) and 3 x 10(-6) M) or SK&F 104353 (10(-6) and 3 x 10(-6) M) (leukotriene antagonists). The contraction was not affected by aspirin (10(-4) M) or indomethacin (10(-6) M) (cyclooxygenase inhibitors), S-1452 (10(-8) M) or ONO-3708 (10(-7) M) (thromboxane A2 antagonists), FR139317 (10(-6) M) (endothelin receptor antagonist) or superoxide dismutase (150 u/ml) combined with catalase (1000 u/ml), or allopurinol (10(-5) M) (antioxidants). In contrast, the endothelium-independent contraction induced by acetylcholine was unaffected by any of these inhibitors and antagonists listed above. The present experiments demonstrate that in the presence of N omega-nitro-L-arginine methyl ester, acetylcholine partly causes an endothelium-dependent contraction in rabbit coronary artery which is probably due to leukotriene C4 and D4, but does not involve production of thromboxane A2, endothelin or superoxide.
authors.affiliation: Pharmacology Division, Kyoto University, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Jino
authors.forename: K
authors.initials: K
authors.lastname: Kurahashi
authors.forename: H
authors.initials: H
authors.lastname: Usui
authors.forename: Y
authors.initials: Y
authors.lastname: Nakata
authors.forename: Y
authors.initials: Y
authors.lastname: Shimizu
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001158:Arteries / Q000187:drug effects* / Q000502:physiology; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D016232:Endothelins / Q000037:antagonists & inhibitors; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D020024:Leukotriene Antagonists; D015289:Leukotrienes / Q000502:physiology*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester; D010741:Phospholipases A / Q000494:pharmacology; D054467:Phospholipases A2; D011817:Rabbits; D013928:Thromboxane A2 / Q000037:antagonists & inhibitors
chemical_list: D000975:Antioxidants; D016232:Endothelins; D020024:Leukotriene Antagonists; D015289:Leukotrienes; D013928:Thromboxane A2; D001120:Arginine; D010741:Phospholipases A; D054467:Phospholipases A2; D019331:NG-Nitroarginine Methyl Ester