[Erythrocyte membrane abnormality of essential hypertension with special reference to membrane fluidity and Na(+)-K+ ATPase activity].

UNLABELLED

To clarify the pathogenesis of essential hypertension (EHT), the biophysical property (fluidity) and Na(+)-K+ ATPase activity of the erythrocyte membrane were pursued. Seventeen patients with EHT, 14 normotensives (NT) with familial history of hypertension and 25 healthy controls (CONTROL) without familial history of hypertension were subjected in this study. Electron spin resonance (ESR) method using 5- or 16-stearic acid label (SAL) was used to measure the membrane fluidity of erythrocytes. Since little changes in the Na(+)-K+ ATPase activity may be expected, the bioluminescence method was adopted to measure the enzyme activity. By evaluation of several measuring conditions for the enzyme activity, the method was revealed to be highly sensitive and reproducible, as has been reported by Lechi. A significant decrease was found in the erythrocyte membrane fluidity of EHT patients using 16-SAL with the parameter of peak height ratio (ho/h-1), when compared with that of CONTROL (EHT: 5.31 +/- 0.13;

CONTROL

5.20 +/- 0.11, p less than 0.05). The decrease of erythrocyte membrane fluidity, values of peak height ratio using 16-SAL, correlated significantly with the systolic blood pressure (r = 0.36 p less than 0.05) and diastolic pressure (r = 0.34 p less than 0.05). The values of peak height ratio of NT (5.26 +/- 0.17) were found in between those of EHT and CONTROL. The levels of erythrocyte membrane Na(+)-K+ ATPase activity in EHT showed higher than those of CONTROL, but the difference was not significant. They did not correlate with the membrane fluidity and the blood pressure. The artificial modifications of membrane cholesterol contents of erythrocytes made the same directional changes in both the membrane fluidity and the enzyme activity. The results showed that the abnormality of biophysical property existed in the deeper portion of the erythrocyte membrane and indicated the possibility of hereditary perpetuation of EHT. As to changes in Na(+)-K+ ATPase activity, no definite contributory relation to EHT has been identified.