Collecting duct–specific gene inactivation of αENaC in the mouse kidney does not impair sodium and potassium balance
J. Clin. Invest. Isabelle Rubera, et al. 112:554 doi:10.1172/JCI16956 [Go to this article.]

Figure 4
Transition of CNT to CCD in the kidney of Scnn1a^loxloxCre and Scnn1a^loxlox mice kept on a sodium-free diet for 6 days. (a) Immunofluorescence on consecutive cryosections with rabbit antibodies against αENaC and AQP2. Bright apical αENaC immunofluorescence ceases abruptly at the transition from CNT to CCD (arrows). AQP2 is seen in CNT and CCD. AQP2-negative cells in CNT and CCD are intercalated cells; the weak, punctuate staining in some tubular cells was not localized at the apical membrane, was occasionally observed with the αENaC antibody, and is nonspecific. P, proximal tubule. Scale bar, ∼20 μm. (b) Immunofluorescent detection of CB, NCX, and αENaC on consecutive cryosections from kidneys of loxlox (control) and loxloxCre (experimental) mice. In mice of both genotypes, the sharp transition from CNT to CCD (arrows) is characterized by a drop of cytoplasmic CB immunostaining and a breakoff, i.e., discontinuity, of basolateral NCX abundance. In the Scnn1a^loxlox mouse, apical αENaC immunostaining continues from the CNT to the CCD, whereas in Scnn1a^loxlox mice, αENaC immunoreactivity is seen in CNT but not CCD. Scale bar, 20 μm.