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Nitric oxide increases persistent sodium current of ventricular myocytes in guinea pig during normoxia and hypoxia

Ma Jihua, Wang Xianpei, Zhang Peihua

Cardio Electrophysiological research Laboratory, Medical college, Wuhan University of Science and Technoloyg. Wuhan 430080, China

Abstract

Whole cell patch-clamp technique was used to record the changes of persistent sodium current (INa.P) and the effect of administered agents in ventricular myocytes of guinea pig to investigate the essence of INa.P and mechanism of increased INa.P of ventricular myocytes during hypoxia. The results showed: (1) Pro-NO L-arginine(L-Arg) and donor sodium nitroprusside (SNP) increased INa.P in a concentration- dependent manner in normoxia. (2) INa.P increased gradually with the prolongation of hypoxia time. After 15 min of hypoxia, administration of N(G)-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, could not significantly recover the increased INa.P [(1.344 ± 320) vs (1.301 ± 0.317) pA/pF, P>0.05, n=5].

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Citing This Article：

Ma Jihua, Wang Xianpei, Zhang Peihua. Nitric oxide increases persistent sodium current of ventricular myocytes in guinea pig during normoxia and hypoxia. Acta Physiol Sin 2004; 56 (5): (in Chinese with English abstract).