Lipid methylation, sodium transport and the response to PTH in renal tubules.

The possible role of progressive methylation of phosphatidylethanolamine to phosphatidylcholine on sodium transport was examined in a suspension of rabbit proximal convoluted tubules. The relation between progressive methylation and the action of parathyroid hormone on sodium transport in this nephron segment was also determined. Incubation of the suspended tubules for 10 minutes at 37 degrees C with 200 microM S-adenosyl-L-[3H]-methyl methionine, a methyl donor, revealed a significant rate of de-novo phosphatidylcholine synthesis. The inactive adenosine analogue, 3-deazaadenosine (DZA), had a significant inhibitory effect on lipid methylation. Despite the inhibition of methylation by DZA, the ouabain sensitive component of oxygen consumption, an index of sodium transport, was not affected. PTH significantly inhibited ouabain sensitive oxygen consumption but had no effect on the methylation of phosphatidylethanolamine. Inhibition of methylation by DZA, did not affect the inhibitory effect of PTH on oxygen consumption. These studies demonstrate that in the proximal convoluted tubule of the rabbit the progressive methylation pathway is present and that inhibition of this pathway does not affect sodium transport. In addition, these studies suggest that the inhibitory effect of PTH on sodium transport is not mediated by the methylation pathway.