AJP - Heart and Circulatory Physiology, Vol 258, Issue 3 766-H772, Copyright © 1990 by American Physiological Society
Electrogenic Na(+)-K+ pump in Purkinje myocytes isolated from control noninfarcted and infarcted hearts
P. A. Boyden and K. P. Dresdner Jr
Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York 10032.
We combined a method of Na+ loading (zero K+ exposure) with voltage-clamp
techniques to determine whether malfunctioning of the Na(+)-K+ pump
underlies the abnormalities in the resting potential and the repolarization
process observed in subendocardial Purkinje cells dispersed from the canine
infarcted ventricle (IZPCs) 24 h after coronary artery occlusion.
Stimulation of the transient outward current (ipump) was produced by a
3-min exposure to zero K+ and then reexposure to 4 mM K+ Tyrode solution.
We compared the properties of ipump in IZPCs to ipump in Purkinje cells
dispersed from fiber strands (SPCs) or from the subendocardium of the
normal hearts (NZPCs). For the holding potentials (mean values: SPC, -33
+/- 7; NZPC, -33 +/- 5; and IZPC, -35 +/- 4 mV), the time constant (tau) of
ipump in IZPCs (55 +/- 18 s) was not significantly different (P greater
than 0.05) from tau in SPCs (55 +/- 10 s) or NZPCs (57 +/- 11 s). Peak
ipump (Imax) and total charge transfer (Q) in IZPCs were not different from
control. In SPCs and NZPCs, there was an increase in Imax and Q when zero
K+ exposure was prolonged to 6-8 min, whereas in some IZPCs, the increase
in Imax or Q was smaller. We conclude that the Na(+)-K+ pump current
kinetics are not altered in IZPCs compared with control. Thus the
persistent electrophysiological abnormalities in IZPCs that can still be
observed after single cell isolation (Boyden, P. A., A. Albala, and K.
Dresdner. Circ. Res. 65: 955-970, 1989) are not explained by an alteration
in the function of the Na(+)-K+ pump.
