Zicha J, Sang K H, Kunes J, Devynck M A
Institute of Physiology, Academy of Sciences of the Czech Republic, Prague.
J Hypertens. 1999 Jun;17(6):785-92. doi: 10.1097/00004872-199917060-00010.
To determine the relationships between blood pressure, membrane microviscosity, plasma lipids and cytosolic pH in Dahl rats susceptible or resistant to salt hypertension.
Blood pressure, plasma triglycerides and total cholesterol, platelet cytosolic pH (pHi) and the microviscosity of both outer membrane leaflet (TMA-DPH fluorescence anisotropy) and membrane lipid core (DPH fluorescence anisotropy) were studied in platelets and erythrocyte ghosts of Dahl salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) rats fed either a low-salt diet (0.3% NaCl) until the age of 9, 15 or 24 weeks or a high-salt diet (4% NaCl) for 5 or 10 weeks after weaning.
At low salt intake, DPH but not TMA-DPH anisotropy increased with age in platelets of SS/Jr rats. Chronic high salt intake was accompanied by an increase of DPH anisotropy in platelets but not in erythrocyte ghosts of SS/Jr rats. Platelet DPH anisotropy correlated positively with blood pressure of salt-loaded SS/Jr rats. Chronic high salt intake also reduced pHi in platelets, the regulation of which seemed to be related to the changes in TMA-DPH anisotropy. This especially concerns the thrombin-induced pHi rise which was inversely related to basal pHi, plasma lipids and TMA-DPH anisotropy. Altered membrane lipid composition might be the underlying mechanism because both membrane microviscosity and platelet pHi regulation were reported to correlate significantly with plasma triglycerides and/or cholesterol.
Platelets of salt hypertensive Dahl rats are characterized by an increased microviscosity of membrane lipid core which correlated positively with blood pressure. The major influence of plasma triglycerides on DPH anisotropy should be taken into consideration when investigating the links between membrane microviscosity and blood pressure. On the other hand, the changes in microviscosity of the outer membrane leaflet might be involved in pHi regulation (probably through control of the Na+/H+ exchanger).
确定对盐性高血压敏感或耐受的 Dahl 大鼠的血压、膜微粘度、血脂与胞质 pH 之间的关系。
在喂食低盐饮食（0.3% NaCl）直至 9、15 或 24 周龄，或断奶后喂食高盐饮食（4% NaCl）5 或 10 周的 Dahl 盐敏感（SS/Jr）和盐抵抗（SR/Jr）大鼠的血小板和红细胞影中，研究血压、血浆甘油三酯和总胆固醇、血小板胞质 pH（pHi）以及外膜小叶（TMA-DPH 荧光各向异性）和膜脂核心（DPH 荧光各向异性）的微粘度。
在低盐摄入时，SS/Jr 大鼠血小板中 DPH 而非 TMA-DPH 各向异性随年龄增加。慢性高盐摄入伴随 SS/Jr 大鼠血小板中 DPH 各向异性增加，但红细胞影中无此现象。血小板 DPH 各向异性与盐负荷的 SS/Jr 大鼠的血压呈正相关。慢性高盐摄入还降低了血小板中的 pHi，其调节似乎与 TMA-DPH 各向异性的变化有关。这尤其涉及凝血酶诱导的 pHi 升高，其与基础 pHi、血脂和 TMA-DPH 各向异性呈负相关。膜脂成分改变可能是潜在机制，因为据报道膜微粘度和血小板 pHi 调节均与血浆甘油三酯和/或胆固醇显著相关。
盐性高血压 Dahl 大鼠的血小板特征为膜脂核心微粘度增加，且与血压呈正相关。在研究膜微粘度与血压之间的联系时，应考虑血浆甘油三酯对 DPH 各向异性的主要影响。另一方面，外膜小叶微粘度的变化可能参与 pHi 调节（可能通过控制 Na+/H+ 交换器）。
