We previously reported that exposure of aquatic-phase Ambystoma tigrinum to a solution containing 50 mM K⁺ (K⁺ adaptation) caused a nearly 10-fold increase in the number of detectable maxi K⁺ channels on the apical membrane of their initial collecting tubules. In apparent contradiction to the notion that maxi K⁺ channels contribute to K⁺ secretion, these channels were not routinely active at the resting membrane potential (0 mV voltage clamp). To test the possibility that hyperkalemia yields maxi K⁺ channels that are secreting K⁺ (i.e., active at 0 mV), we patch-clamped the apical membranes of initial collecting tubules under conditions of elevated basolateral K⁺ (15 mM). Seven patches containing maxi K⁺ channels were studied. Six of the seven patches showed maxi K⁺ channel activity when voltage was clamped at 0 mV. Open probability and unitary current averaged 0.059 ± 0.016 and 1.65 ± 0.50 pA, respectively. This activity, together with the high density of channels observed (1.06 channels/µm²), indicates that after K⁺ adaptation, maxi K⁺ channels contribute to the ability of the late distal nephron of amphibians to secrete K⁺.

amphibian collecting tubule; homeostatic K⁺ secretion; K⁺ adaptation; hyperkalemic conditions

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