Altered delayed rectifier K+ current of rabbit coronary arterial myocytes in isoproterenol-induced hypertrophy.
- Author:
Nari KIM
1
;
Jin HAN
;
Euiyong KIM
Author Information
1. Department of Physiology and Biophysics, College of Medicine, Inje University, 633-165 Gaegum-dong, Busanjin-gu, Busan, South Korea. phykimey@ijnc.inje.co.kr
- Publication Type:Original Article
- Keywords:
Potassium channels;
Isoproterenol;
Hypertrophy;
Coronary;
Patch clamp technic
- MeSH:
Cardiomegaly;
Heart;
Hypertrophy*;
Isoproterenol;
Kinetics;
Membranes;
Muscle Cells*;
Myocytes, Smooth Muscle;
Potassium Channels
- From:The Korean Journal of Physiology and Pharmacology
2001;5(1):33-40
- CountryRepublic of Korea
- Language:English
-
Abstract:
The aim of present study was to define the cellular mechanisms underlying changes in delayed rectifier K+ (KDR) channel function in isoproterenol-induced hypertrophy. It has been proposed that KDR channels play a role in regulation of vascular tone by limiting membrane depolarization in arterial smooth muscle cells. The alterations of the properties of coronary KDR channels have not been studied as a possible mechanism for impaired coronary reserve in cardiac hypertrophy. The present study was carried out to compare the properties of coronary KDR channels in normal and hypertrophied hearts. These channels were measured from rabbit coronary smooth muscle cells using a patch clamp technique. The main findings of the study are as follows: (1) the KDR current density was decreased without changes of the channel kinetics in isoproterenol-induced hypertrophy; (2) the sensitivity of coronary KDR channels to 4-AP was increased in isoproterenol-induced hypertrophy. From the above results, we suggest for the first time that the alteration of KDR channels may limit vasodilating responses to several stimuli and may be involved in impaired coronary reserve in isoproterenol-induced hypertrophy.
