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Hypotonic Shock Modulates Na+ Current via a Cl- and Ca2+/Calmodulin Dependent Mechanism in Alveolar Epithelial Cells

Figure 4

Implication of Cl- channels and KCC in basal and hypotonic-induced transepithelial current.

Basal transepithelial current (Isc Basal), hypotonic-induced current (Isc 20% Hypo) and the current rise elicited by hypotonic shock (Δ Isc Shock) are depicted in the basal conditions (Ctrl), after treatment with 100 µM basolateral bumetanide (Bumet), 100 µM apical (NPPBa) or basolateral (NPPBb) NPPB, in bilateral Cl- reduced buffer (Cl-(-)) or 100 µM basolateral DIOA. In experiments where the cells were pre-treated with an inhibitor that impacted on Isc, hypotonic shock was induced when the current was stabilized. For apical and basolateral NPPB, a 5 to 10 min incubation was needed while the current stabilized after ~30 min for DIOA. Pre-treatment with bumetanide from 10 min to 30 min did not have an impact on Isc Basal. N≥4, *p<0.05 by Mann-Whitney Test compared to untreated controls. # p<0.05 by Mann-Whitney Test compared to NPPBa, ¤ p<0.05 by Mann-Whitney Test compared to NPPBb or DIOA.

Figure 4