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. 2012 Feb 1;302(10):C1436–C1451. doi: 10.1152/ajpcell.00063.2011

Fig. 6.

Fig. 6.

Pharmacologic assessment of basolateral Na+-stimulated acid extrusion in cilium-deficient and -competent cell monolayers. A: cariporide-sensitive pHi recovery from an acid load in cilium-deficient monolayers. The experimental protocol and data presentation are similar to that shown in Fig. 5A. Returning basolateral Na+ elicited the expected pHi increase (ab), which was reduced by 1 μM cariporide (ab′), and almost eliminated by 50 μM cariporide (ab″). B: HOE-694-sensitive pHi recovery from an acid load in cilium-deficient monolayers. The experimental protocol was similar to that shown in A, except with the NHE inhibitor HOE-694. Returning basolateral Na+ elicited the expected pHi increase (ab), which was reduced by 10 μM HOE-694 (ab′) and eliminated by 100 μM HOE-694 (ab″). C: cariporide sensitivity of basolateral Na+-induced acid extrusion in cilium-deficient monolayers. Data from panel A-type experiments with Fig. 5B-type analyses were used to calculate the pHi dependencies of total acid extrusion (♦), 1 μM cariporide-insensitive acid extrusion (■), and 50 μM cariporide-insensitive acid extrusion (▴); n ≥ 3 for each symbol. D: cariporide sensitivity of basolateral Na+-induced acid extrusion in cilium-competent monolayers; n ≥ 3 for each symbol.