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细胞膜微粘度和钙镁ATP酶活性与自发性高血压大鼠模型的高血压无关。

Cell membrane microviscosity and Ca(2+)-Mg(2+)-ATPase activity do not contribute to hypertension in the spontaneously hypertensive rat model.

作者信息

Norman R I, Achall N

机构信息

Department of Medicine, University of Leicester, U.K.

出版信息

Clin Sci (Lond). 1993 Nov;85(5):585-91. doi: 10.1042/cs0850585.

Abstract
  1. The relationships between systolic blood pressure and altered erythrocyte Ca(2+)-Mg(2+)-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. Ca(2+)-Mg(2+)-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 Ca(2+)-Mg(2+)-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 Ca(2+)-Mg(2+)-ATPase activity and membrane microviscosity are causally unrelated to hypertension in these animals.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 本研究评估了收缩压与红细胞钙镁 -ATP 酶活性及膜微黏度改变之间的关系。实验所用膜样本取自 20 周龄雌性 Wistar - Kyoto 正常血压大鼠和自发性高血压大鼠,这些大鼠来自两个不同来源(Charles River 和 Harlan OLAC),以及由 Wistar - Kyoto 大鼠与来自一个来源(Charles River)的自发性高血压大鼠杂交产生的第二代(F2)。2. 来自两个来源的自发性高血压大鼠的收缩压均显著高于 Wistar - Kyoto 动物(P < 0.05;Charles River 组为 151 ± 4 和 110 ± 3 mmHg;Harlan OLAC 组为 155 ± 4 和 122 ± 4 mmHg)。F2 大鼠群体的收缩压范围在 73 至 168 mmHg 之间。3. 钙镁 -ATP 酶活性通过测量依赖 ATP 的 45Ca2+ 摄取到内翻囊泡中的量来测定,微黏度通过测量膜结合荧光探针(包括 1,6 - 二苯基 -1,3,5 - 己三烯、三甲氨基 -1,6 - 二苯基 -1,3,5 - 己三烯和一系列蒽氧基脂肪酸)的偏振各向异性来评估。4. 与先前研究相反,通过比较自发性高血压大鼠和 Wistar - Kyoto 动物,或分析 F2 大鼠群体,未发现成年收缩压与红细胞钙镁 -ATP 酶活性或总体或局部膜微黏度之间存在关联。5. 这些结果表明,钙镁 -ATP 酶活性和膜微黏度与这些动物的高血压并无因果关系。(摘要截断于 250 字)

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