title: The Na+-activated K+ channel contributes to K+ efflux in Na+-loaded guinea-pig but not rat ventricular myocytes.
abstract: Activation of the Na+-activated K+ channels (KNa channels) has been suggested to contribute to the ischaemia-induced accumulation of extracellular K+ (K+e) in the mammalian myocardium. Recent evidence shows that these channels are not present in rat ventricular myocytes [9]. We have therefore investigated the effect of raised intracellular Na+ activity (aiNa) on intracellular K+ activity (aiK) in guinea-pig myocytes, which possess the channels, and on rat ventricular myocytes which do not. The Na+-activated K+ current was activated by an increase in aiNa induced by removing extracellular Ca2+ and Mg2+ and inhibiting the Na-pump. The aiNa increased and the aiK decreased in both guinea-pig and rat myocytes superfused with Ca2+- and Mg2+-free Tyrode. The new steady-state increase in aiNa and decline in aiK were similar in both species. Inhibition of the Na-pump resulted in an additional increase in aiNa and decrease in aiK in both species. However, both the increase in aiNa and decrease in aiK were greater in guinea-pig myocytes and the decline in aiK in guinea-pig myocytes followed the development of a large Na+-activated K+ current. When Li+ replaced Na+ in the superfusate the Na+-activated K+ current did not develop and the fall in aiK was reduced. In Na+-loaded rat myocytes, which do not have a Na+-activated K+ current, the decline in aiK was reduced and blocked by 2 mM Mg2+ suggesting that a Mg2+-sensitive non-specific cation channel may be involved in the K+ efflux from rat myocytes [12]. These data suggest that KNa channels are a major route for K+ efflux from Na+-loaded guinea-pig myocytes.
authors.affiliation: Department of Physiology, Otago Medical School, University of Otago, Dunedin, New Zealand.
authors.forename: C L
authors.initials: CL
authors.lastname: Lawrence
authors.forename: G C
authors.initials: GC
authors.lastname: Rodrigo
mesh_terms: D000818:Animals; D002118:Calcium / Q000494:pharmacology; D006168:Guinea Pigs; D006352:Heart Ventricles / Q000166:cytology / Q000378:metabolism; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000378:metabolism*; D017202:Myocardial Ischemia / Q000378:metabolism; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012982:Sodium, Dietary / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013045:Species Specificity
chemical_list: D015221:Potassium Channels; D012982:Sodium, Dietary; D000254:Sodium-Potassium-Exchanging ATPase; D008274:Magnesium; D011188:Potassium; D002118:Calcium