Altered electrophysiological properties of coronary artery in isoprenaline-induced cardiac 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, 614-735, South Korea. phykimey@ijnc.inje.ac.kr
- Publication Type:Original Article
- MeSH:
Cardiomegaly*;
Coronary Vessels*;
Hypertrophy;
Hypertrophy, Left Ventricular;
Kinetics;
Microscopy, Electron;
Myocytes, Smooth Muscle;
Noise;
Patch-Clamp Techniques;
Rabbits;
Relaxation;
Tea
- From:The Korean Journal of Physiology and Pharmacology
2001;5(5):413-421
- CountryRepublic of Korea
- Language:English
-
Abstract:
An impaired smooth muscle cell (SMC) relaxation of coronary artery by alteration of K+ channels would be the most potential explanation for reduced coronary reserve in left ventricular hypertrophy (LVH), however, this possibility has not been investigated. We performed morphometrical analysis of the coronary artery under electron microscopy and measured Ca2+-activated K (KCa) currents and delayed rectifier K (Kdr) currents by whole-cell and inside-out patch-clamp technique in single coronary arterial SMCs from rabbits subjected to isoprenaline-induced cardiac hypertrophy. Coronary arterial SMCs underwent significant changes in ultrastructure. The unitary current amplitude and the open-state probability of KCa channel were significantly reduced in hypertrophy without open-time and closed-time kinetic. The concentration-response curve of KCa channel to Ca2+ is shifted to the right in hypertrophy. The reduction in the mean single channel current and increase in the open channel noise of KCa channel by TEA were more sensitive in hypertrophy. Kdr current density is significantly reduced in hypertrophy without activation and inactivation kinetics. The sensitivity of Kdr current on 4-AP is significantly increased in hypertrophy. This is the first study to report evidence for alterations of KCa channels and Kdr channels in coronary SMCs with LVH. The findings may provide some insight into mechanism of the reduced coronary reserve in LVH.
