Relations of sodium-lithium countertransport kinetics to plasma and red cell membrane phospholipids in hyperlipidemia.

As compared to 7 normolipidemic donors, the maximal velocity of sodium-lithium countertransport was accelerated by nearly 70% in 10 patients with elevated levels of triglyceride-rich lipoproteins and tended to be stimulated also in 5 patients with hypercholesterolemia. No significant differences were observed between normolipidemia and both hyperlipidemic groups for the apparent affinities of the transport system for intracellular sodium and extracellular lithium. Strong positive relations of the maximal activity of sodium-lithium countertransport to the percentages of red cell membrane phosphatidylcholine (r = 0.85, 2P < 0.001), the phosphatidylcholine/sphingomyelin (r = 0.82, 2P < 0.001) and the phosphatidylcholine/phosphatidylethanolamine ratio (r = 0.81, 2P < 0.001) were seen in all donors. A negative correlation was found to membrane sphingomyelin (r = -0.72, 2P < 0.001). Also plasma phosphatidylcholine and sphingomyelin exhibited positive and negative associations, respectively, to the maximal activity of sodium-lithium countertransport (r = 0.66, 2P < 0.01 and r = -0.78, 2P < 0.001). Among several plasma lipoprotein parameters investigated, total triglycerides or VLDL cholesterol levels showed independent relations to both the plasma and the membrane phosphatidylcholine/sphingomyelin ratio as well as to the maximal velocity of sodium-lithium countertransport. The results indicate that an increase in red cell membrane phosphatidylcholine and a concomitant fall in sphingomyelin are closely associated with the acceleration of sodium-lithium countertransport in hyperlipidemia.