OBJECTIVE: The Na+ activated K+ channel (IK(Na)) may be activated during ischaemia when the intracellular Na+ concentration is raised. As ischaemia is also associated with intracellular acidification, the influence of intracellular pH on this K+ channel was investigated. METHODS: The effects of intracellular Na+ and H+ on the IK(Na) channel were investigated in isolated patches from guinea pig ventricular myocytes by the patch clamp technique. RESULTS: Increase of intracellular Na+ increased the open probability of the channel. Intracellular acidification had no effect on the single channel conductance, but significantly decreased the open probability of the channel in the pH range 7.5-6.5. The effect of intracellular pH on open probability was about the same in a wide range of intracellular Na+ concentrations. The lower open probability induced by acidification seemed to be caused by prolonged closed times. CONCLUSIONS: Because the effects of increased intracellular Na+ and decreased pH on open probability are opposite, it is suggested that the IK(Na) channel might be important under conditions of raised intracellular Na+ with relatively unchanged intracellular pH. Consequently, it is hypothesised that this channel may be involved in adaptation of action potential duration at high heart rate and in action potential shortening in the border zone of regional ischaemic areas.
OBJECTIVE: The Na+ activated K+ channel (IK(Na)) may be activated during ischaemia when the intracellular Na+ concentration is raised. As ischaemia is also associated with intracellular acidification, the influence of intracellular pH on this K+ channel was investigated. METHODS: The effects of intracellular Na+ and H+ on the IK(Na) channel were investigated in isolated patches from guinea pig ventricular myocytes by the patch clamp technique. RESULTS: Increase of intracellular Na+ increased the open probability of the channel. Intracellular acidification had no effect on the single channel conductance, but significantly decreased the open probability of the channel in the pH range 7.5-6.5. The effect of intracellular pH on open probability was about the same in a wide range of intracellular Na+ concentrations. The lower open probability induced by acidification seemed to be caused by prolonged closed times. CONCLUSIONS: Because the effects of increased intracellular Na+ and decreased pH on open probability are opposite, it is suggested that the IK(Na) channel might be important under conditions of raised intracellular Na+ with relatively unchanged intracellular pH. Consequently, it is hypothesised that this channel may be involved in adaptation of action potential duration at high heart rate and in action potential shortening in the border zone of regional ischaemic areas.