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 (V̇max) 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 V̇max could be observed under Ca-free condition too. Increase of V̇max caused by 10-7 m Ni2+ was not prevented by cholinergic blockade (atropine, 3×10-7 m) by β-adrenergic blockade (pindolol, 4×10-7 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 V̇max 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∞-curve relating V̇max of the ventricular action potential to the membrane potential was increased by 10-7 m Ni2+. The increase of V̇max 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 V̇max was shifted by 5 mV to more negative potentials by 10-7 m Ni2+. Our results suggest that nickel ions in low concentration increase the sodium conductance in the heart by an unknown mechanism and influence the inactivation process of the fast Na+ channel.
- Beta-adrenergic blocker
- Ca-free solution
- Cardiac transmembrane action potential
- Nickel ions
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine