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Titolo:
Importance of glycolytically derived ATP for Na+ loading via Na+/H+ exchange during metabolic inhibition in guinea pig ventricular myocytes
Autore:
Satoh, H; Sugiyama, S; Nomura, N; Terada, H; Hayashi, H;
Indirizzi:
Hamamatsu Univ, Sch Med, Div Cardiol, Hamamatsu, Shizuoka 4313192, Japan Hamamatsu Univ Hamamatsu Shizuoka Japan 4313192 , Shizuoka 4313192, Japan
Titolo Testata:
CLINICAL SCIENCE
fascicolo: 3, volume: 101, anno: 2001,
pagine: 243 - 251
SICI:
0143-5221(200109)101:3<243:IOGDAF>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARDIAC PURKINJE-FIBER; ISCHEMIC RAT-HEART; H+ EXCHANGE; INTRACELLULAR NA+; CYTOPLASMIC ATP; GROWTH-FACTORS; CALCIUM; CELLS; DEPENDENCE; ANTIPORT;
Keywords:
glycolysis; metabolic inhibition; myocytes; Na+/H+ exchange; sodium;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Satoh, H Hamamatsu Univ, Sch Med, Div Cardiol, 1-20-1 Handayama, Hamamatsu, Shizuoka 4313192, Japan Hamamatsu Univ 1-20-1 Handayama Hamamatsu Shizuoka Japan 4313192
Citazione:
H. Satoh et al., "Importance of glycolytically derived ATP for Na+ loading via Na+/H+ exchange during metabolic inhibition in guinea pig ventricular myocytes", CLIN SCI, 101(3), 2001, pp. 243-251

Abstract

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 ispredominantly 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 similar to 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 beforerigor 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 toactivate 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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Documento generato il 23/01/20 alle ore 18:21:07