title: Testosterone causes simultaneous decrease of [Ca2+]I and tension in rabbit coronary arteries: by opening voltage dependent potassium channels.
abstract: The relationship between the level of testosterone and the incidence of coronary heart disease is still controversial in the view of the results of clinical and epidemiologic studies. This uncertainty might be partly due to relatively small number of experimental studies undertaken to investigate the cellular mechanism underlying the vascular responses to testosterone. To further investigate the cellular mechanisms of testosterone with respect to vascular response, we investigated the effect of testosterone on contractility and intracellular Ca2+ regulation in a rabbit coronary artery and evaluated the underlying mechanism of testosterone-induced changes of coronary vascular tone by using various pharmacological blockers. Testosterone was found to relax rabbit coronary arteries in a dose-dependent manner, and no significant difference was found in the relaxation response to testosterone with or without endothelium. Similar results were obtained in male and non-pregnant female rabbit coronary arteries. The relaxation response of rabbit coronary arteries to testosterone was greater for PGF2alpha-contracted rings than for KCl contracted rings, which suggest the involvement of K+ channels. Furthermore, the relaxation response to testosterone was significantly reduced by 4-aminopyridine, a sensitive blocker of voltage dependent K+ channels, but not by low doses of tetraethylammonium or iberiotoxin, a Ca2+ activated K+ channel blocker. Testosterone simultaneously reduced the intracellular Ca2+ concentration ([Ca2+]i) and tension, and 4-AP effectively antagonized the testosterone-induced change of [Ca2+]i and tension. Therefore, it may be concluded that the stimulation of voltage dependent K channels is responsible, at least in part, for the testosterone-induced relaxation of rabbit coronary arteries.
authors.affiliation: Department of Physiology, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Eunkyoung
authors.initials: E
authors.lastname: Won
authors.forename: Jongeun
authors.initials: J
authors.lastname: Won
authors.forename: Seongchun
authors.initials: S
authors.lastname: Kwon
authors.forename: Youngho
authors.initials: Y
authors.lastname: Lee
authors.forename: Taickzsang
authors.initials: T
authors.lastname: Nam
authors.forename: Ducksun
authors.initials: D
authors.lastname: Ahn
mesh_terms: D000728:Androgens / Q000494:pharmacology*; D000818:Animals; D001158:Arteries / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D003331:Coronary Vessels / Q000187:drug effects*; D005260:Female; D007425:Intracellular Membranes / Q000378:metabolism*; D008297:Male; D009994:Osmolar Concentration; D024642:Potassium Channels, Voltage-Gated / Q000187:drug effects / Q000378:metabolism*; D011817:Rabbits; D013739:Testosterone / Q000494:pharmacology*; D014664:Vasodilation
chemical_list: D000728:Androgens; D024642:Potassium Channels, Voltage-Gated; D013739:Testosterone; D002118:Calcium