B. Engelmann et al., RELATIONS OF SODIUM-LITHIUM COUNTERTRANSPORT KINETICS TO PLASMA AND RED-CELL MEMBRANE PHOSPHOLIPIDS IN HYPERLIPIDEMIA, Atherosclerosis, 99(2), 1993, pp. 151-163
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 signifi
cant differences were observed between normolipidemia and both hyperli
pidemic groups for the apparent affinities of the transport system for
intracellular sodium and extracellular lithium. Strong positive relat
ions 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) a
nd the phosphatidylcholine/phosphatidylethanolamine ratio (r = 0.81, 2
P < 0.001) were seen in all donors. A negative correlation was found t
o membrane sphingomyelin (r = -0.72, 2P < 0.001). Also plasma phosphat
idylcholine and sphingomyelin exhibited positive and negative associat
ions, respectively, to the maximal activity of sodium-lithium countert
ransport (r = 0.66, 2P < 0.01 and r = -0.78, 2P < 0.001). Among severa
l plasma lipoprotein parameters investigated, total triglycerides or V
LDL cholesterol levels showed independent relations to both the plasma
and the membrane phosphatidylcholine/sphingomyelin ratio as well as t
o the maximal velocity of sodium-lithium countertransport. The results
indicate that an increase in red cell membrane phosphatidylcholine an
d a concomitant fall in sphingomyelin are closely associated with the
acceleration of sodium-lithium countertransport in hyperlipidemia.