Cardioprotective drugs decrease the Na+ background current.
10.3349/ymj.1995.36.3.278
- Author:
So Ra PARK
1
;
Gul Ha RYU
;
Chang Kook SUH
Author Information
1. Department of Physiology, Inha University College of Medicine, Inchon, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Background current;
myocardial protein;
amiloride;
R 56865
- MeSH:
Amiloride/pharmacology;
Animal;
Guinea Pigs;
Heart/*drug effects;
Heart Arrest, Induced;
Myocardium/metabolism;
Piperidines/pharmacology;
Potassium/pharmacology;
Sodium/*metabolism;
Support, Non-U.S. Gov't;
Thiazoles/pharmacology;
Verapamil/pharmacology
- From:Yonsei Medical Journal
1995;36(3):278-286
- CountryRepublic of Korea
- Language:English
-
Abstract:
Cardiac dysfunctions such as myocardial functional failure and ventricular arrhythmia have been largely attributed to intracellular Ca2+ overload. One of the mechanisms of intracellular Ca2+ overload involves a rapid influx of Ca2+ via Na(+)-Ca2+ exchange during the reperfusion which utilizes the accumulation of Na+ in myocytes during ischemic cardiac arrest. Possible sources of the intracellular Na+ accumulation include Na+ channel, Na(+)-H+ exchange, Na(+)-Ca2+ exchange, and Na+ background current. In this study, we studied the role of the Na+ background current in intracellular Na+ accumulation during the cardiac arrest by measuring the Na+ background current in guinea pig ventricular myocytes with whole cell clamp method and evaluating the effects of cardioprotective drugs on the Na+ background current. The results were as follows: (1) The Na+ background inward current at -40 mV membrane potential was larger at Ca2+ free solution than 1.8 mM Ca2+ solution. (2) The Na+ background current was not affected by verapamil. (3) 2 microM O-(N, N-hexamethylene)-amiloride (HMA) decreased the Na+ background current at negative membrane potential. (4) The new cardioprotective drug, R 56865, decreased the Na+ background current. These results suggest that the Na+ background current plays a role in increasing the intracellular Na+ activity during high K+ cardioplegia and the blocking effect of myoprotective drugs, such as R 56865, on the Na+ background current may contribute to myocardial protection after cardioplegia.
