Regulative effects of temperature, intracellular sodium, ATP and pH on I(Na/Ca) of cardiac myocytes.
- Author:
Hong-Yi ZHOU
1
;
Chong-Yang HAN
;
Xiao-Liang WANG
Author Information
1. Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
- Publication Type:Journal Article
- MeSH:
Adenosine Triphosphate;
physiology;
Animals;
Calcium;
metabolism;
Guinea Pigs;
Heart Ventricles;
cytology;
pathology;
Hydrogen-Ion Concentration;
Hypoxia;
physiopathology;
Intracellular Fluid;
physiology;
Male;
Myocytes, Cardiac;
metabolism;
physiology;
Patch-Clamp Techniques;
Sodium;
physiology;
Sodium-Calcium Exchanger;
physiology;
Temperature
- From:
Acta Physiologica Sinica
2006;58(2):136-140
- CountryChina
- Language:Chinese
-
Abstract:
The Na(+)-Ca(2+) exchange is a major pathway for removal of cytosolic Ca(2+) in cardiac myocytes. To explore the effects of temperature, intracellular Na(+), ATP and pH on Na(+)-Ca(2+) exchange currents (I(Na/Ca)) of intact guinea-pig myocytes, the whole-cell patch-clamp technique was used to record I(Na/Ca) in isolated guinea-pig ventricular myocytes. We found that I(Na/Ca) at 34 degrees C was four times higher than that at 22 degrees C. However, intracellular acidification had no obvious influence on bidirectional I(Na/Ca). At 22~24 degrees C , intracellular ATP depletion and intracellular acidification did not markedly affect bidirectional I(Na/Ca) either. At 34~37 degrees C , intracellular ATP depletion and intracellular acidification synergistically inhibited the outward and inward currents of I(Na/Ca), and blocked the inward currents of I(Na/Ca)more potently than the outward currents of I(Na/Ca). The effect of ATP on I(Na/Ca) is temperature-dependent. Intracellular higher sodium increased the outward currents of I(Na/Ca) however it did not increase, even sometimes decreased the inward currents of I(Na/Ca). These results suggest that intracellular ATP depletion and intracellular acidification synergistically impair Ca(2+) extrusion via forward mode Na(+)-Ca(2+) exchange, and intracellular sodium overload increases Ca(2+) influx via reverse mode Na(+)-Ca(2+) exchange, leading to calcium overload respectively.
