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.
Dausch
R
R
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.
Spring
K R
KR
D000818:Animals; D002034:Bumetanide / Q000494:pharmacology; D004847:Epithelial Cells; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism; D005704:Gallbladder / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009338:Necturus maculosus; D010042:Ouabain / Q000494:pharmacology; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism*; D012965:Sodium Chloride / Q000378:metabolism*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D002034:Bumetanide; D012965:Sodium Chloride; D010042:Ouabain; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate