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Testosterone Causes Simultaneous Decrease of [Ca2+]i and Tension in Rabbit Coronary Arteries: by Opening Voltage Dependent Potassium Channels

Authors
 Eun Kyoung Won  ;  Jong Eun Won  ;  Duck Sun Ahn  ;  Taick Sang Nam  ;  Young Ho Lee  ;  Seong Chun Kwon 
Citation
 YONSEI MEDICAL JOURNAL, Vol.44(6) : 1027-1033, 2003 
Journal Title
 YONSEI MEDICAL JOURNAL 
ISSN
 0513-5796 
Issue Date
2003
MeSH
Testosterone ; voltage dependent K^+ channels ; rabbit coronary artery ; 4-aminopyridine ; intracellular ca^(2+)
Keywords
Testosterone ; voltage dependent K^+ channels ; rabbit coronary artery ; 4-aminopyridine ; intracellular ca^(2+)
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 PGF2α-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.
Files in This Item:
T200303485.pdf Download
DOI
OAK-2003-00423
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Nam, Taick Sang(남택상)
Ahn, Duk Sun(안덕선) ORCID logo https://orcid.org/0000-0001-9351-6951
Lee, Young Ho(이영호) ORCID logo https://orcid.org/0000-0002-5749-1045
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/113583
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