Effects of nickel ions on the transmembrane action potential of guinea-pig heart preparations.

Experiments in isolated left auricle and right ventricular papillary muscle from guinea-pig hearts were performed in order to study the effects of nickel ions (Ni2+) on the transmembrane action potential. On the electrically paced guinea-pig left auricle NiCl2 in 10(-8)M concentration did not modify the action potential (AP). 10(-7)M Ni2+ caused a slight hyperpolarizing effect, markedly enhanced the maximum rate of rise of AP (Vmax) and shortened the duration of AP.10(-6) and 10(-5)M NiCl2 dose-dependently accelerated the repolarization, while 10(-5)M had a strong depolarizing effect, too. The stimulatory effect of 10(-7)M NiCl2 on Vmax could be observed under Ca-free condition too. Increase of Vmax caused by 10(-7)M Ni2+ was not prevented by cholinergic blockade (atropine, 3 X 10(-7)M) by beta-adrenergic blockade (pindolol, 4 X 10(-7)M) or by inhibition of prostaglandin synthesis (indomethacin, 10(-6)M). On the electrically paced guinea-pig papillary muscle both 10(-7)M and 10(-5)M NiCl2 increased the resting membrane potential (RP), the overshoot and Vmax but accelerated only slightly the initial repolarization phase. A concentration of 10(-4)M NiCl2, however, without causing any effect on the other parameters, shortened the whole repolarization phase. The h infinity-curve relating Vmax of the ventricular action potential to the membrane potential was increased by 10(-7)M Ni2+. The increase of Vmax was more pronounced at membrane potentials more negative than -75 mV and could not be observed at membrane potentials more positive than -70 mV. Steady state inactivation of Vmax was shifted by 5 mV to more negative potentials by 10(-7)M Ni2+.(ABSTRACT TRUNCATED AT 250 WORDS)