Stimulation by high external potassium of the sodium efflux in barnacle muscle fibers.
Single barnacle muscle fibers from Balanus nubilus were used to study the effect of elevated external potassium concentration, [K]o, on Na efflux, membrane potential, and cyclic nucleotide levels. Elevation of [K]o causes a prompt, transient stimulation of the ouabain-insensitive Na efflux. The minimal effective concentrations is  mM. The membrane potential of ouabain-treated fibers bathed in 10 mM Ca2+ artificial seawater (ASW) or in Ca2+-free ASW decreases approximately linearly with increasing logarithm of [K]o. The slope of the plot is slightly steeper for fibers bathed in Ca2+-free ASW. The magnitude of the stimulatory response of the ouabain-insensitive Na efflux to 100 mM Ko depends on the external Na+ and Ca2+ concentrations, as well as on external pH, but is independent of external Mg2+ concentration. External application of 10(-4) M verapamil virtually abolishes the response of the Na efflux to subsequent K-depolarization. Stabilization of myoplasmic-free Ca2+ by injection of 250 mM EGTA before exposure of the fiber to 100 mM Ko leads to approximately 60% reduction in the magnitude of the stimulation. Pre-injection of a pure inhibitor of cyclic AMP-dependent protein kinase reduces the response of the Na efflux to 100 mM Ko by  50%. Increasing intracellular ATP, by injection of 0.5 M ATP-Na2 before elevation of [K]o, fails to prolong the duration of the stimulation of the Na efflux. Exposure of ouabain-treated, cannulated fibers to 100 mM Ko for time periods ranging from 30 sec to 10 min causes a small (approximately 60%), but significant, increase in the intracellular content of cyclic AMP with little change in the cyclic GMP level. These results are compatible with the view that the stimulatory response of the ouabain-insensitive Na efflux to high Ko is largely due to a fall in myoplasmic pCa resulting from activation of voltage-dependent Ca2+ channels and that an accompanying rise in internal cAMP accounts for a portion of this response.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000067956:Adenylyl Cyclase Inhibitors; D000818:Animals; D002118:Calcium / Q000502:physiology*; D002614:Chelating Agents / Q000494:pharmacology; D007473:Ion Channels / Q000502:physiology*; D008274:Magnesium / Q000494:pharmacology; D009132:Muscles / Q000502:physiology*; D009712:Nucleotides, Cyclic / Q000378:metabolism; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology*; D047428:Protein Kinase Inhibitors; D012964:Sodium / Q000378:metabolism*; D001468:Thoracica / Q000502:physiology*; D014700:Verapamil / Q000494:pharmacology
D000067956:Adenylyl Cyclase Inhibitors; D002614:Chelating Agents; D007473:Ion Channels; D009712:Nucleotides, Cyclic; D047428:Protein Kinase Inhibitors; D010042:Ouabain; D000255:Adenosine Triphosphate; D012964:Sodium; D014700:Verapamil; D008274:Magnesium; D011188:Potassium; D002118:Calcium