Kir4.1/Kir5.1, in the basolateral membrane of the early DCT (DCT1) in both wild-type (WT) and cav-1-knockout (KO) mice. However, the activity of this basolateral 40-pS K + channel was lower in KO mice than in WT mice. Moreover, the K + reversal potential (an indication of membrane potential) was less negative in the DCT1 of KO mice than in the DCT1 of WT mice. Western blot analysis demonstrated that cav-1 deficiency decreased the expression of the Na + /Cl -cotransporter and Ste20-proline-alanine-rich kinase (SPAK) but increased the expression of epithelial Na + channel-a. Furthermore, the urinary excretion of Mg 2+ and K + was significantly higher in KO mice than in WT mice, and KO mice developed hypomagnesemia, hypocalcemia, and hypokalemia. We conclude that disruption of cav-1 decreases basolateral K + channel activity and depolarizes the cell membrane potential in the DCT1 at least in part by suppressing the stimulatory effect of c-Src on Kcnj10. Furthermore, the decrease in Kcnj10 and Na + /Cl -cotransporter expression induced by cav-1 deficiency may underlie the compromised renal transport of Mg 2+ , Ca 2+ , and K + .