14 24

Cited 0 times in

Mechanisms of relaxation of coronary artery by hypoxia

 Young Ho Lee  ;  Joung Taek Kim  ;  Bok Soon Kang 
 YONSEI MEDICAL JOURNAL, Vol.39(3) : 252-260, 1998 
Journal Title
Issue Date
Animals ; Coronary Vessels/drug effects ; Coronary Vessels/physiopathology* ; Cyclooxygenase Inhibitors/pharmacology ; Enzyme Inhibitors/pharmacology ; Female ; Hypoxia/physiopathology* ; Indomethacin/pharmacology ; Male ; Nitroarginine/pharmacology ; Rabbits ; Tetraethylammonium/pharmacology ; Vasodilation/physiology*
This study was designed to clarify the dependency of hypoxic coronary vasodilation (HCD) on the endothelium and the role of the K+ channels on HCD in the rabbit coronary artery. HCD was investigated in an isolated left circumflex coronary artery precontracted with prostaglandin F2 α. Vascular rings were suspended for isometric tension recording in an organ chamber filled with Krebs-Henseleit (KH) solution. Hypoxia was induced by gassing the chamber with 95% N2 + 5% CO2 and was maintained for 15 approximately 25 min. Hypoxia elicited a vasodilation in the precontracted coronary artery with and without endothelium. There was no difference between the amplitude of the HCD induced by two consecutive hypoxic challenges and the effects of 20% O2 + 5% CO2 + 75% N2 and 95% O2 + 5% CO2 control K-H solution of subsequent responses to hypoxia. Inhibition of the cyclooxygenase pathway by treatment with indomethacin had no effect on HCD. Blockades of the tetraethylammonium chloride-sensitive K+ channel abolished HCD. Apamin, a blocker of the small conductance Ca2+-activated K+ (KCa) channel, and iberiotoxin, a blocker of the large conductance KCa channel had no effect on HCD, respectively. Glibenclamide, a blocker of the ATP-sensitive K+ (K+ATP) channel, reduced HCD. Cromakalim, an opener of the K+ATP channel, relaxed the coronary artery precontracted with prostaglandin F2 α. The degree of relaxation by cromakalim was similar to that by hypoxia while glibenclamide reduced both hypoxia- and cromakalim-induced vasodilatations. In conclusion, these results suggest that HCD is independent on endothelium and HCD is considered to be induced by activation of K+ATP channel.
Files in This Item:
T199801745.pdf Download
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Lee, Young Ho(이영호) ORCID logo https://orcid.org/0000-0002-5749-1045
사서에게 알리기


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.