Ca2+-dependent Long-term Inactivation of Cardiac Na+/Ca2+ Exchanger
The Korean Journal of Physiology and Pharmacology
; : 183-188, 2007.
Article
in English
| WPRIM (Western Pacific)
| ID: wpr-728209
Responsible library:
WPRO
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.
Full text:
Available
Database:
WPRIM (Western Pacific)
Main subject:
Capsaicin
/
Calcium
/
Cytoplasm
/
Cytosol
Language:
English
Journal:
The Korean Journal of Physiology and Pharmacology
Year:
2007
Document type:
Article