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 for 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 non-ciliary origin. Immunoperfusion of isolated and fixed CCDs isolated from control K⁺ fed rabbits with channel subunit-specific Abs 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 for 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 pharmacologic deciliation suggests that cilia BK channels do not contribute to K⁺ secretion in this segment, but that cilia serve as modulators of cell signaling.