Erythrocyte membrane microviscosity and blood pressure in rats with salt‐induced and spontaneous hypertension
作者:
Jaroslav Kunes,
Josef Zicha,
Marie-Aude Devynck,
期刊:
Journal of Hypertension
(OVID Available online 1994)
卷期:
Volume 12,
issue 3
页码: 229-234
ISSN:0263-6352
年代: 1994
出版商: OVID
关键词: Sabra rat;inbred Dahl rat;Lyon rat;genetic hypertension;diphenylhexatriene;trimethylamino-diphenylhexatriene;fluorescence anisotropy;erythrocyte membrane;blood pressure
数据来源: OVID
摘要:
ObjectiveTo study membrane viscosity in various rat strains with genetic forms of experimental hypertension.DesignThe relationship between blood pressure and membrane dynamics was investigated in erythrocytes from three different rat strains with experimental hypertension, namely two models of salt-induced hypertension (Sabra and Dahl rats) and Lyon hypertensive rats with spontaneous hypertension.MethodsMembrane microviscosity was evaluated by diphenylhexatriene and trimethylamino-diphenylhexatriene fluorescence steady-state anisotropy.ResultsThere were no significant differences among particular experimental groups in trimethylamino-diphenylhexatriene anisotropy that reflect micro-viscosity changes at the water-lipid interface of the external membrane leaflet. In contrast, the diphenylhexatriene anisotropy, which is related to the core membrane microviscosity, was significantly reduced in the Dahl salt-sensitive rats (irrespective of salt intake level) and in the Sabra hypertension-prone rats with developed salt hypertension. Erythrocyte membranes of Lyon hypertensive rats also had lower values of diphenylhexatriene anisotropy than the respective normotensive controls but this difference was not statistically significant.ConclusionsSystolic (and often also diastolic) blood pressure correlated negatively with the diphenylhexatriene anisotropy in each of the three strains studied, whereas the trimethylamino-diphenylhexatriene anisotropy of the erythrocyte membranes had no significant relationship to the blood pressure. Further experiments should clarify whether the observed relationship of the diphenylhexatriene anisotropy to blood pressure reflects true pathogenetic mechanisms or is a consequence of haemodynamic changes.
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