INHIBITION OF SODIUM-PLUS-POTASSIUM-STIMULATED ADENOSINE-TRIPHOSPHATASE (NA-K+-ATPASE) BY PROTEIN-KINASE-C ACTIVATORS IN THE GILLS OF ATLANTIC COD (GADUS-MORHUA)()

Exogenous (phorbol ester) and endogenous (diacylglycerol) activators o f protein kinase C (PKC) inhibited sodium efflux across the gills of A tlantic cod Gadus morhua and inhibited sodium-plus-potassium-stimulate d adenosine triphosphatase (Na+-K+-ATPase) in isolated chloride cells. The branchial sodium efflux measured in a perfused whole-body prepara tion was inhibited by 47% on administration of 10(-6) mol.L(-1) phorbo l 12, 13-dibutyrate (PDB). The branchial perfusion pressure was increa sed by 46% by 10(-6) mol.L(-1) PDB. In contrast the synthetic diacylgl ycerol, 1-oleoyl-2-acetyl gycerol (GAG) did not alter significantly pe rfusion pressure but did reduce sodium efflux by 13% at a concentratio n of 4 x 10(-6) mol.L(-1). The effects of these agents on Na+-K+-ATPas e activity were determined in isolated chloride cells with a control a ctivity of 30.9 +/- 1.9 mu mol Pi mg protein(-1) hour(-1). PDB and OAG both inhibited enzyme activity in a dose-dependent manner, with 10(-5 ) mol.L(-1) causing 45% and 26% inhibition, respectively. These result s suggest that PKC is involved in regulating sodium efflux in the gill s of cod by modulating Na+-K(+)ATPase activity.