Fig. 4.

Aldosterone induces ATP release and changes the morphology of A6 cells. (A) Effect of control (n = 8), aldosterone (n = 8), and basolateral hypotonic stress (n = 7) on the amiloride-sensitive transepithelial electrical conductance (G_t^ENaC) of A6 cell monolayer. (B) Rate of ATP release (R_ATP) from A6 cell monolayers during control (n = 7), aldosterone stimulation (n = 7), and basolateral hypotonic stress (n = 5). All data in A and B were expressed as the average of experiments (mean ± SE.). Asterisk denotes value statistically different from the control based on Student's t test (*, P < 0.05). (C) Effect of basolateral ATPγS on the topography of A6 cells. Shown are two SICM topographical images of a selected area of a living A6 cell monolayer before (Control) and after (+ATP) stimulation with ATPγS. (D) Effect of ATPγSonG_t of A6 cell monolayer. ATPγS (50 μM) was added to basolateral side. (E) Effect of hexokinase on the aldosterone-induced G_t of A6 cell monolayer. Aldosterone and hexokinase/glucose were added together to the basolateral compartment at the time marked by the arrow, and then the hexokinase/glucose was removed 90 min later. (F) Hexokinase and glucose were added to the basolateral compartment of an aldosterone-stimulated A6 cell monolayer at the time marked by the arrow (Upper). DPCPX (100 nM), a P1 receptor antagonist, was added to the basolateral compartment of an aldosterone-stimulated A6 cell monolayer at the time marked by the arrow (Lower). The thick lines on the bottom of D, E, and F indicate the application of amiloride to the apical side of the A6 cell monolayer.