Heterogeneity of the SR-dependent Inward Na+-Ca2+ Exchange Current in the Heavily Ca2+-buffered Rat Ventricular Myocytes.
- Author:
Kyung Bong YOON
1
;
Sung Wan AHN
;
Chang Mann KO
Author Information
1. Department of Anesthesiology, Yonsei University Wonju College of Medicine, Wonju 220-701, S. Korea.
- Publication Type:Original Article
- Keywords:
Voltage-sensitive release mechanism;
Ca2+-induced Ca2+ release;
Heavy Ca2+-buffering;
Na+- Ca2+ exchange;
SR;
Rat heart
- MeSH:
Action Potentials;
Animals;
Cadmium Chloride;
Cytosol;
Muscle Cells*;
Population Characteristics*;
Rats*;
Ryanodine Receptor Calcium Release Channel;
Tetracaine
- From:The Korean Journal of Physiology and Pharmacology
2004;8(2):101-110
- CountryRepublic of Korea
- Language:English
-
Abstract:
Voltage-sensitive release mechanism was pharmacologically dissected from the Ca2+-induced Ca2+ release in the SR Ca2+ release in the rat ventricular myocytes patch-clamped in a whole-cell mode. SR Ca2+ release process was monitored by using forward-mode Na+-Ca2+ exchange after restriction of the interactions between Ca2+ from SR and Na+-Ca2+ exchange within micro-domains with heavy cytosolic Ca2+ buffering with 10 mM BAPTA. During stimulation every 10 s with a pulse roughly mimicking action potential, the initial outward current gradually turned into a huge inward current of -12.9+/-0.5 pA/pF. From the inward current, two different inward INCXs were identified. One was 10 muM ryanodine-sensitive, constituting 14.2+/-2.3%. It was completely blocked by CdCl2 (0.1 mM and 0.5 mM) and by Na+-depletion. The other was identified by 5 mM NiCl2 after suppression of ICaL and ryanodine receptor, constituting 14.8+/-1.6%. This latter was blocked by either 10 mM caffeine-induced SR Ca2+-depletion or 1 mM tetracaine. IV-relationships illustrated that the latter was activated until the peak in 30~35 mV lower voltages than the former. Overall, it was concluded that the SR Ca2+ release process in the rat ventricular myocytes is mediated by the voltage-sensitive release mechanism in addition to the Ca2+-induced-Ca2+ release.
