The cortical collecting duct (CCD) is a final site for regulation of K⁺ homeostasis. CCD K⁺ secretion is determined by the electrochemical gradient and apical permeability to K⁺. Conducting secretory K⁺ (SK/ROMK) and maxi-K channels are present in the apical membrane of the CCD, the former in principal cells and the latter in both principal and intercalated cells. Whereas SK channels mediate baseline K⁺ secretion, maxi-K channels appear to participate in flow-stimulated K⁺ secretion. Chronic dietary K⁺ loading enhances the CCD K⁺ secretory capacity due, in part, to an increase in SK channel density (Palmer et al., J Gen Physiol 104: 693–710, 1994). Long-term exposure of Ambystoma tigrinum to elevated K⁺ increases renal K⁺ excretion due to an increase in apical maxi-K channel density in their CDs (Stoner and Viggiano, J Membr Biol 162: 107–116, 1998). The purpose of the present study was to test whether K⁺ adaptation in the mammalian CCD is associated with upregulation of maxi-K channel expression. New Zealand White rabbits were fed a low (LK), control (CK), or high (HK) K⁺ diet for 10–14 days. Real-time PCR quantitation of message encoding maxi-K α- and β_2–4-subunits in single CCDs from HK animals was greater than that detected in CK and LK animals (P < 0.05); β₁-subunit was not detected in any CCD sample but was present in whole kidney. Indirect immunofluorescence microscopy revealed a predominantly intracellular distribution of α-subunits in LK kidneys. In contrast, robust apical labeling was detected primarily in α-intercalated cells in HK kidneys. In summary, K⁺ adaptation is associated with an increase in steady-state abundance of maxi-K channel subunit-specific mRNAs and immunodetectable apical α-subunit, the latter observation consistent with redistribution from an intracellular pool to the plasma membrane.