Potassium loss from rabbit myocardium during hypoxia: evidence for passive efflux linked to anion extrusion.

To determine the effects of permeant and impermeant anions and of osmolarity on potassium (K+) exchange, the net uptake and efflux of 42K+ were recorded in the isolated arterially perfused rabbit septum. Perfusion with solution made hyperosmolar by adding NaCl (30 mM) or sucrose (60 mM) caused similar increases of 42K+ uptake which were reversible on returning to the control solution. Washout experiments showed that the loss of K+ on returning to the control perfusate was due to a decreased influx probably mediated by inhibition of the sodium pump. The effects of anions were studied by replacing chloride in the control solution with the inert and impermeant substitute isethionate (114 mM) or by loading the myocardium with sodium dimethyloxazeolidinedione (NaDMO, 30 mM) under isosmotic condition and switching to a perfusate containing sodium isethionate (30 mM). In both these conditions a reduction of 42K content could be detected and was attributable to an increased efflux. During hypoxic substrate free perfusion K+ loss was due to an increased efflux with no evidence for altered influx of potassium. The extrusion of accumulated anions from the myocardium could be the major determinant of the early potassium loss during hypoxia and ischaemia.