Importance of electrogenic sodium pump in normal and overdriven sinoatrial pacemaker

Abstract

Automatic cardiac cells can be electrically paced so that action potentials occur at a rate substantially faster than their normal spontaneous rate. Immediately following the cessation of pacing the spontaneous rate falls temporarily. This phenomenon of “overdrive suppression” or “postpacing inhibition” in atrial pacemakers has been previously attributed to acetylcholine release from autonomic nerve endings by the pacing stimulation. The experiments reported here were performed on strips of tissue from the dominant sinoatrial pacemaker of rabbit heart in the presence of 1.4 to 2.8 μ m atropine to block acetylcholine receptors. Under such conditions postpacing inhibition is still observed, but can be reversibly abolished by brief application of 10 −5 m ouabain. Ouabain application also produces a temporary increase in the spontaneous beat rate of sinoatrial node strips and is able to block the rate reduction observed when K + is restored after K +-free perfusion. The results suggest that a significant component of postpacing inhibition in rabbit sinoatrial node is due to an electrogenic Na + pump and that pacemaker rate can be directly affected by alterations in pump activity.