Korean J Physiol Pharmacol.
2001 Oct;5(5):413-421.
Altered electrophysiological properties of coronary artery in
isoprenaline-induced cardiac hypertrophy
- Affiliations
-
- 1Department 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
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.