Within the CCD of the distal nephron of the rabbit, the BK (maxi K) channel mediates Ca²⁺- and/or stretch-dependent flow-induced K⁺ secretion (FIKS) and contributes to K⁺ adaptation in response to dietary K⁺ loading. An unresolved question is whether BK channels in intercalated cells (ICs) and/or principal cells (PCs) in the CCD mediate these K⁺ secretory processes. In support of a role for ICs in FIKS is the higher density of immunoreactive apical BKα (pore-forming subunit) and functional BK channel activity than detected in PCs, and an increase in IC BKα expression in response to a high-K⁺ diet. PCs possess a single apical cilium which has been proposed to serve as a mechanosensor; direct manipulation of cilia leads to increases in cell Ca²⁺ concentration, albeit of nonciliary origin. Immunoperfusion of isolated and fixed CCDs isolated from control K⁺-fed rabbits with channel subunit-specific antibodies revealed colocalization of immunodetectable BKα- and β1-subunits in cilia as well as on the apical membrane of cilia-expressing PCs. Ciliary BK channels were more easily detected in rabbits fed a low-K⁺ vs. high-K⁺ diet. Single-channel recordings of cilia revealed K⁺ channels with conductance and kinetics typical of the BK channel. The observations that 1) FIKS was preserved but 2) the high-amplitude Ca²⁺ peak elicited by flow was reduced in microperfused CCDs subject to pharmacological deciliation suggest that cilia BK channels do not contribute to K⁺ secretion in this segment, but that cilia serve as modulators of cell signaling.