[Effect of acute hypoxia on L-type calcium current of the ventricular myocytes of guinea-pig].

When the conventional whole cell recording technique is used to study the inward calcium current in cardiac cells, the "Run down" phenomenon of calcium channel would prevent sufficient time of recording desirable for adequate experimental analysis. The "Run down" phenomenon could be minimized by using nystatin-whole cell recording technique in isolated guinea-pig ventricular cells. The inward L-type calcium current could be maintained at a steady level for up to more than 100 min, showing the presence of an endogenous steady calcium ion buffering mechanism. With nystatin-whole cell recording, the L-type calcium current after 10 min acute hypoxia (Po2 4 +/- 0.7 kPa) was inhibited (peak amplitude decreased) and the I-V relation was shifted upward. The inward calcium current showed no recovery after 10 min reoxygenation. The peak amplitude was lower than that of the control. The results suggested that the decrease of action potential duration (APD) under acute hypoxia was not only due to increase of outward potassium current, but also a decrease of inward calcium current. All these phenomena may be related to some inhibition of phosphorylation of the L-type calcium channel in the cardiac cells under hypoxia.