Basolateral membrane potassium conductance is independent of sodium pump activity and membrane voltage in canine tracheal epithelium

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Abstract
When secretagogues stimulate Cl secretion in canine tracheal epithelium, apical membrane Cl conductance (G a Cl ) increases, and then basolateral membrane K conductance (G b K ) increases. Conversely, inhibition ofG a Cl results in a secondary decrease inG b K . The coordination of the two membrane conductances and regulation ofG b K is critical for maintaining constant intracellular ion concentrations and transepithelial Cl secretion. The purpose of this study was to test two hypotheses about the regulation ofG b K . First, we asked whetherG b K is directly linked to the activity of the Na,K-ATPase. We found that pump activity could be dissociated from K conductance. Inhibition of the Na pump with ouabain, in nonsecreting tissues led to an increase inG b . Elevation of the bathing solution K concentration produced a similar effect. Addition of ouabain to secreting tissues did not appear to alterG b . These results indicate thatG b K does not directly parallel Na pump activity. Second, we asked whether changes inG b K are voltage dependent. We prevented secretagogue-induced depolarization of the electrical potential difference across the basolateral membrane Ψ b by clamping Ψ b at its resting value during stimulation of Cl secretion with epinephrine. Despite maintaining Ψ b constant, the typical changes in transepithelial resistance and the ratio of membrane resistances persisted. This observation indicates that depolarization is not required for the secretagogue-induced increase inG b K . In addition we examined the effect of depolarizing and hyperpolarizing Ψ b by passing transepithelial current in secreting and nonsecreting epithelia. Despite depolarizing and hyperpolarizing Ψ b within the physiologic range, we observed no significant changes in transepithelial resistance or the ratio of membrane resistance that would suggest a change inG b K . This observation indicates that changes in Ψ b are not sufficient to alterG b K . Thus,G b K appears to be regulated by factors other than membrane voltage, or direct coupling to the Na pump.