Cell Membrane Microviscosity and Ca²⁺-Mg²⁺-ATPase Activity do Not Contribute to Hypertension in the Spontaneously Hypertensive Rat Model

1. The relationships between systolic blood pressure and altered erythrocyte Ca²⁺-Mg²⁺-ATPase activity and membrane microviscosity were assessed in membranes prepared from 20-week-old female Wistar-Kyoto normotensive and spontaneously hypertensive rats obtained from two different sources (Charles River and Harlan OLAC) and a second filial (F₂) generation derived from a cross between Wistar-Kyoto rats and spontaneously hypertensive rats from one source (Charles River).

2. Spontaneously hypertensive rats from both sources had systolic blood pressures significantly higher than those of Wistar-Kyoto animals (P <0.05; 151 + 4 and 110 + 3 mmHg, Charles River; 155 + 4 and 122 + 4 mmHg, Harlan OLAC). The systolic blood pressures for the F₂ rat population ranged between 73 and 168 mmHg.

3. Ca²⁺-Mg²⁺-ATPase activity was measured as ATP-dependent ⁴⁵Ca²⁺ uptake into inside-out vesicles and microviscosity assessed by the measurement of polarization anisotropy of membrane incorporated fluorescent probes including 1,6-diphenyl-1,3,5-hexatriene, trimethylamino-1,6-diphenyl-1,3,5-hexatriene and a series of anthroyloxy fatty acids.

4. Contrary to previous studies, no relationship between adult systolic blood pressure and erythrocyte Ca²⁺-Mg²⁺-ATPase activity or general or localized membrane microviscosity was indicated by the comparison of spontaneously hypertensive and Wistar-Kyoto animals or in the analysis of the F₂ rat population.

5. These results suggest that Ca²⁺-Mg²⁺-ATPase activity and membrane microviscosity are causally unrelated to hypertension in these animals. On the assumption that biophysical properties of the erythrocyte membrane reflect those of smooth muscle, our results suggest that membrane alteration does not play a significant role in the pathogenesis of hypertension in the spontaneously hypertensive rat model.