Contribution of sodium channel and sodium/hydrogen exchanger to sodium accumulation in the ischemic myocardium.
Contribution of sodium channels and sodium/hydrogen exchangers (NHEs) to sodium accumulation during ischemia in the ischemic/reperfused heart was examined. Ischemia increased the myocardial sodium. Reperfusion elicited a further increase in the myocardial sodium, which was associated with little recovery of the left ventricular developed pressure (LVDP) of the perfused heart. Treatment with tetrodotoxin or dimethylamirolide (DMA) dose-dependently attenuated the ischemia- and reperfusion-induced increase in myocardial sodium and enhanced the post-ischemic recovery of the LVDP. There was an inverse relationship between the increase in myocardial sodium during ischemia and the post-ischemic recovery of the LVDP.The myocardial sodium accumulation during ischemia is mainly attributed to sodium influx through sodium channels and NHEs.
Tanonaka
K
K
Department of Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Tokyo 192-0392, Hachioji, Japan.
Takasaki
A
A
Kajiwara
H
H
Takeo
S
S
D000584:Amiloride / Q000031:analogs & derivatives* / Q000494:pharmacology; D000818:Animals; D066298:In Vitro Techniques; D007477:Ions / Q000378:metabolism; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism*; D026941:Sodium Channel Blockers; D015222:Sodium Channels / Q000378:metabolism*; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000187:drug effects
D007477:Ions; D026941:Sodium Channel Blockers; D015222:Sodium Channels; D017923:Sodium-Hydrogen Exchangers; C039465:5-dimethylamiloride; D013779:Tetrodotoxin; D000584:Amiloride; D012964:Sodium