A vascular smooth muscles nitric oxide relaxation by a mechanism distinct of calcium changes

• Published in: Life sciences (1973) Vol. 54; no. 19; p. 1449
• Main Authors: Chabaud, F, Danna, M, Bény, J L
• Format: Journal Article
• Language: English
• Published: Netherlands 1994
• Subjects: Acetylcholine - pharmacology; Animals; Arginine - analogs & derivatives; Arginine - pharmacology; Bradykinin - pharmacology; Calcimycin - pharmacology; Calcium - metabolism; Coronary Vessels - drug effects; Coronary Vessels - metabolism; Coronary Vessels - physiology; Cytosol - metabolism; Dinoprost - pharmacology; Egtazic Acid - pharmacology; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiology; Fura-2; In Vitro Techniques; Indomethacin - pharmacology; Ionomycin - pharmacology; Isometric Contraction - drug effects; Isometric Contraction - physiology; Muscle Relaxation - drug effects; Muscle Relaxation - physiology; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - metabolism; Muscle, Smooth, Vascular - physiology; Nitric Oxide - physiology; Nitroarginine; Nitroglycerin - pharmacology; Potassium - pharmacology; Spectrometry, Fluorescence; Substance P - pharmacology; Swine
• ISSN: 0024-3205
• DOI: 10.1016/0024-3205(94)00600-8

Prostaglandin F2 alpha contracts coronary arteries smooth muscles under conditions of extra cellular and intracellular calcium depletion. In these conditions, nitrogen-oxide-containing vasodilators or natural EDRF(s) released by the kinins, substance P and bradykinin, from the endothelium relax strips of pig coronary arteries. This indicates that nitric oxide not only needs to lower cytosolic free calcium to relaxes the smooth muscles, but in addition another mechanism, independent of cytosolic calcium changes, is necessary to fully relax strips contracted by Prostaglandin F2 alpha.