Effects of adenosine on transmembrane potential and sarcolemmal Na+-K+ ATPase activity of human atrial myocardium.

Abstract

Adenosine effects on the transmembrane potential characteristics and the sarcolemmal Na+-K+ ATPase activity of human atrial myocardium were studied in tissue from 20 patients who were divided into 2 groups based on the maximum diastolic potentials (MDP) greater than or less than -60 mV. Group A consisted of 10 patients with MDP of 70.84 +/- 4.20 mV and Na+-K+ ATPase activity of 15.37 +/- 0.46 mumole Pi/mg/hr. Ten patients with MDP of 44.54 +/- 6.24 mV and Na+-K+ ATPase activity of 12.55 +/- 0.42 mumole Pi/mg/hr were included in group B. Adenosine had no effects on the electrophysiological properties and the sarcolemmal Na+-K+ ATPase activity of atrial myocardium at concentrations below 1 X 10(-5) M in either group. Adenosine resulted in mildly altered atrial transmembranes potentials without significant effect on Na+-K+ ATPase activity at concentrations between 1 X 10(-5) M and 5 X 10(-4) M. However, a significant reduction of transmembrane potentials and an apparent inhibition of Na+-K+ ATPase activity were observed only in tissue from group B. These results suggest that: 1) adenosine has no effect on the electrophysiological properties and the sarcolemmal Na+-K+ ATPase activity of human atrial myocardium at physiological concentrations; 2) adenosine induced inhibition of the sarcolemmal Na+-K+ ATPase activity in slow channel-dependent atrial tissues may be a mechanism responsible for the alterations of transmembrane potentials under unphysiological conditions; and 3) adenosine contributes to the genesis of cardiac arrhythmias during acute myocardial ischemia, which can reduce transmembrane potentials of the myocardial cells and may increase the myocardial adenosine level above its effective concentration.