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. 2012 Jul 9;590(Pt 21):5273–5297. doi: 10.1113/jphysiol.2012.236893

Figure 11. Inhibitor effects suggest basal Ieq and HCO3 secretion depend on CFTR and on Ca2+-dependent, membrane-bound adenylyl cyclase activity, but not on HCO3 -stimulated soluble adenylyl cyclase.

Figure 11

A, basal Ieq was abolished by apical addition of the CFTR open channel blocker GlyH-101 (100 μmol l−1, n= 4). B, basal Ieq and net HCO3 secretion were inhibited by bilateral addition of 200 μmol l−1 Rp-cAMPS, a competitive inhibitor of cAMP-dependent PKA (n= 4). C, basal Ieq and HCO3 secretion were reduced by basolateral MDL-12330A (200 μmol l−1), an inhibitor of membrane-bound adenylyl cyclase (n= 4). D, inhibition of basal Ieq and HCO3 secretion by apical 2-APB (100 μmol l−1), an inhibitor of store-operated Ca2+ channels (n= 3). E, an inhibitor of HCO3-stimulated soluble isoform of adenylyl cyclase, 2-HE (20 μmol l−1), had no effect on Ieq or HCO3 secretion (n= 3 each) when added bilaterally. F, summary of inhibitor effects on basal anion transport. ▪, Ieq; □, HCO3 secretion.