Regulation of NaCl entry into Necturus gallbladder epithelium by protein kinase C

The role of protein kinase C in the regulation of the mode of NaCl entry into Necturus gallbladder epithelial cells was determined from the rate and magnitude of ouabain-induced cell swelling in the presence of inhibitors. Stimulation of protein kinase C by phorbol ester increased the rate of cell swelling from the control value of 2.9% to 4.7%/min and caused the predominant apical membrane transport mechanism for NaCl to switch from bumetanide-sensitive Na-Cl cotransport to amiloride-sensitive parallel exchange. Na-Cl cotransport could be restored as the predominant mode of NaCl entry by treatment of stimulated tissues with the kinase inhibitors 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) and calphostin C. Therefore the mechanism of NaCl transport across the apical membrane can be controlled by the activity of protein kinase C.