Intracellular acidosis decreases the outward Na+-Ca2+exchange current in guinea pig ventricular myocytes

1995 ◽  
Vol 36 (2) ◽  
pp. 146 ◽  
Author(s):  
Ek Ho Lee ◽  
So Ra Park ◽  
Kwang Se Paik ◽  
Chang Kook Suh
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Exchange Current ◽  
Intracellular Acidosis

scholarly journals Inhibitory effect of aprindine on Na+ /Ca2+ exchange current in guinea-pig cardiac ventricular myocytes

2002 ◽  
Vol 136 (3) ◽  
pp. 361-366 ◽  
Author(s):  
Yasuhide Watanabe ◽  
Takahiro Iwamoto ◽  
Munekazu Shigekawa ◽  
Junko Kimura
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inhibitory Effect ◽  
Exchange Current ◽  
Cardiac Ventricular Myocytes

scholarly journals Inhibitory Effect of Cibenzoline on Na+/Ca2+ Exchange Current in Guinea-Pig Cardiac Ventricular Myocytes

2012 ◽  
Vol 120 (1) ◽  
pp. 59-62 ◽  
Author(s):  
Tomomi Yamakawa ◽  
Yasuhide Watanabe ◽  
Hiroshi Watanabe ◽  
Junko Kimura
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inhibitory Effect ◽  
Exchange Current ◽  
Cardiac Ventricular Myocytes

scholarly journals Inhibitory effect of 2,3-butanedione monoxime (BDM) on Na+ /Ca2+ exchange current in guinea-pig cardiac ventricular myocytes

2001 ◽  
Vol 132 (6) ◽  
pp. 1317-1325 ◽  
Author(s):  
Yasuhide Watanabe ◽  
Takahiro Iwamoto ◽  
Isao Matsuoka ◽  
Satoko Ohkubo ◽  
Tomoyuki Ono ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inhibitory Effect ◽  
Exchange Current ◽  
Butanedione Monoxime ◽  
Cardiac Ventricular Myocytes

scholarly journals Regulation kinetics of Na + ‐Ca 2+ exchange current in guinea‐pig ventricular myocytes

2000 ◽  
Vol 529 (3) ◽  
pp. 611-623 ◽  
Author(s):  
Yasutada Fujioka ◽  
Koh Hiroe ◽  
Satoshi Matsuoka
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Exchange Current ◽  
Kinetics Of

Importance of glycolytically derived ATP for Na+ loading via Na+/H+ exchange during metabolic inhibition in guinea pig ventricular myocytes

2001 ◽  
Vol 101 (3) ◽  
pp. 243-251 ◽  
Author(s):  
Hiroshi SATOH ◽  
Shiho SUGIYAMA ◽  
Noriyuki NOMURA ◽  
Hajime TERADA ◽  
Hideharu HAYASHI
Keyword(s):  
Guinea Pig ◽  
Myocardial Ischaemia ◽  
Cell Injury ◽  
Ventricular Myocytes ◽  
Metabolic Inhibition ◽  
Intracellular Acidosis ◽  
Major Pathway ◽  
Intracellular Atp ◽  
Rate Of Increase ◽  
Inhibition Of Glycolysis

The increase in the intracellular Na+ concentration ([Na+]i) during myocardial ischaemia is crucial for ischaemia/reperfusion cell injury, and the cardiac subtype of the Na+/H+ exchanger (NHE-1) has been shown to be a major pathway for Na+ loading. While the importance of glycolytically derived ATP for the optimal functioning of membrane transporters and channels has been suggested, whether NHE-1 is actually activated during myocardial ischaemia remains controversial. Here we examined whether the activity of NHE-1 is predominantly dependent on intracellular ATP generated by glycolysis, and whether the additional inhibition of glycolysis can affect the increase in [Na+]i during the inhibition of oxidative phosphorylation in intact guinea pig ventricular myocytes. The selective inhibition of glycolysis by 2-deoxyglucose prevented the recovery of intracellular pH and the transient increase in [Na+]i following intracellular acidosis induced by a NH4Cl pre-pulse. During severe metabolic inhibition (SMI; induced by amobarbital and carbonyl cyanide m-chlorophenylhydrazone in a glucose-free perfusate), most myocytes changed from rod-shaped to contracted forms by ~ 15 min. [Na+]i increased linearly until rigor contracture occurred, but after rigor contracture the rate of increase was blunted. The increase in [Na+]i during SMI was suppressed significantly by an inhibitor of NHE-1, hexamethylene amiloride. The increase in the intracellular Mg2+ concentration, which can reciprocally indicate depletion of intracellular ATP, was small during the initial 10 min of SMI, but became larger from just a few minutes before rigor contracture. In the presence of 2-deoxyglucose, the time to rigor during SMI was shortened, but the increase in [Na+]i before rigor contracture was not significant, and was much less than that in the absence of 2-deoxyglucose. It is concluded that ATP generated by glycolysis is essential to activate NHE-1, and that the dependence of NHE-1 on glycolysis might affect the increase in [Na+]i observed during myocardial ischaemia.

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