토끼 동방결절 세포의 Delayed Rectifier K+ 전류에 미치는 이가 양이온의 차단효과

Abstract

In sinoatrial(SA) node cells, K+ conductance increases only when the membrane is depolarized and the delayed rectifier K+ current, ik, is activated. This leads to repolarizaion which in turn induces the deactivation of channel, causing the membrane potential to depolarize once again towards the threshold of the action potential. Therefore the decay of ik plays a key role in the pacemaker depolarizaion. In the present study, we have investigated the effects of divalent cations(Ni²+, Ba²+, Co²+, and Mn²+) on the delayed rectifier K current in rabbit SA node cells using the whole cell votage clamp technique. CsCl(2 mM) was added to block the hyperpolarizaion activated inward current(ir). K+ currents were recorded in ligh K+ (140 mM) solution. When divalent cations were added to a control solution, they reduced both the instantaneous and the steady-state values of currents recorded on hyperpolarizaion. The blockade was potential-dependent, and steady-state currents were significantly reduced with increasing hyperpolarizaion. The inward currents that recorded during hyperpolarizing voltage steps were relaxed exponetially with time as the blockade by divalent cations developed. Increased the concentraion of the divalent cations elevated the rate of the blockade at a given potential. These phenomena were highly sensitive to temperature, suggesting the presence of ionic binding sites on the channel. Inward K+ currents measured at-80 mV after various depolarizing prepulses(-10 to -40mV) were increased in the more depolarizing prepulses, and showed the steady-state blocking evidence at 0.1 mM Ni²+. Ni²+, Ba²+, Co²+, and Mn²+ had a similar effect, but the velocity of the blocking action is slightly different from one another(Ni²+>Co²+>Mn²+>Ba²+).