Ca2+-dependent Long-term Inactivation of Cardiac Na+/Ca2+ Exchanger.
- Author:
Jee Eun LEE
1
;
Tong Mook KANG
Author Information
1. Department of Physiology, SBRI, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea. tmkang@yurim.skku.ac.kr
- Publication Type:Original Article
- Keywords:
Na+/Ca2+ exchange;
Calcium;
Inactivation;
TRPV1;
BHK cell
- MeSH:
Calcium;
Capsaicin;
Cytoplasm;
Cytosol
- From:The Korean Journal of Physiology and Pharmacology
2007;11(5):183-188
- CountryRepublic of Korea
- Language:English
-
Abstract:
Using BHK cells with stable expression of cardiac Na+/Ca2+ exchanger (BHK-NCX1), reverse mode (i.e. Ca2+ influx mode) of NCX1 current was recorded by whole-cell patch clamp. Repeated stimulation of reverse NCX1 produced a cytosolic Ca2+-dependent long-term inactivation of the exchanger activity. The degrees of inactivation correlated with NCX1 densities of the cells and were attenuated by reduced Ca2+ influx via the reverse exchanger. The inactivation of NCX1 was attenuated by (i) inhibition of Ca2+ influx with reduced extracellular Ca2+, (ii) treatment with NCX1 blocker (Ni2+), and (iii) increase of cytoplasmic Ca2+ buffer (EGTA). In BHK-NCX1 cells transiently expressing TRPV1 channels, Ca2+ influx elicited by capsaicin produced a marked inactivation of NCX1. We suggest that cytoplasmic Ca2+ has a dual effect on NCX1 activities, and that allosteric Ca2+ activation of NCX1 can be opposed by the Ca2+-dependent long-term inactivation in intact cells.
