This study evaluated the effect of L-1-oleoyl-2-acetoyl sn-3-glycerol (OAG) on ouabain-sensitive Na,K-depen dent oxygen consumption (Na,K-QO2) in intact renal proximal tubule cells (RPTC). Basal Na,K-QO2 (nmol O2/mg protein per min) was 20.0±1.0. Incubation with 10 nM of OAG induced a dual effect on Na,K-QO2, with an initial stimulation (maximal at 10 min, 37.1±5.0), followed by an inhibition (significant at 20 min, 16.3±1.0). No changes in ouabain-insensitive QO2 were observed in any of the protocols. The effects were abolished by sphingosine, a protein kinase C inhibitor. Stimulation was abolished by amHorlde 0.1 mM. Amiloride had no effect on Na,K-QO2 at the concen tration used. Stimulation was not potentiated by the sodium ionophore, amphotericine B, and the later inhibition was still observed in the presence of ampho tericine B. The initial stimulation was attributed to an increase in sodium permeability, while the later inhi bition was attributed to a direct effect on the Na,K pump. Regulation of Na+,K+-ATPase activity by pro tein kinase C in intact RPTC can be accomplished by a direct effect on the protein or as a secondary effect consequent upon changes in intracellular sodium.

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