Increased membrane sphingomyelin and arachidonic acid in stroke-prone spontaneously hypertensive rats

Cell membrane composition and fluidity are altered in hypertension. Previous reports suggest arachidonic acid, a metabolically active fatty acid, is increased in the membranes of hypertensive animals compared to control. This increase in unsaturated fatty acids does not explain the observed reduction in fluidity in hypertensive rats, suggesting some other factors affecting fluidity may be present. It has been suggested that the metabolism of sphingomyelin is altered in genetic hypertension. We hypothesized that membrane sphingomyelin content is increased in hypertensive animals.

Stroke-prone spontaneously hypertensive rats (n = 8) were compared with Wistar-Kyoto rats (n = 8). Erythrocyte membranes were prepared and the lipids extracted and separated. Fatty acid methyl esters were produced, identified, and quantified by gas chromatography-mass spectrometry; membrane lipid content was also assessed.

The concentration of sphingomyelin was higher in the membrane of the hypertensive rats (45.7+/-6 v 22.4+/-2 microg/mg of protein) compared to control. The previously observed increase in membrane arachidonic acid content was observed in hypertensive animals when compared to control (130+/-32 v 40+/-3 microg/mg of protein). However, this difference was confined to the phosphatidylinositol (18+/-4 v 6.5+/-1.5 microg/mg of protein) and free fatty acid (2.1+/-0.4 v 0.6+/-0.1 microg/mg of protein) fractions.

We hypothesize that reports of reduced membrane fluidity observed in hypertension may be due to an increase in the proportion of sphingomyelin in the cell membrane.