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自发性高血压大鼠血清对培养的血管平滑肌细胞中⁸⁶Rb洗脱的影响。

Effect of serum from spontaneously hypertensive rats on 86Rb washout in cultured vascular smooth muscle cells.

作者信息

Kuriyama S, Nakamura K, Tokutome G, Kaguchi Y, Hashimoto T, Sakai O

机构信息

Second Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan.

出版信息

Acta Cardiol. 1990;45(1):35-43.

PMID:2316303
Abstract

In addition to the known genetic abnormalities affecting the membrane permeability of vascular smooth muscle cells (VSMC) of spontaneously hypertensive rats (SHR), serum humoral factors may also play some role in the alteration of permeability of VSMC and possibly contribute to the pathogenesis of hypertension in SHR. To test this hypothesis, the passive K permeability described as the washout rate constant (Ke) was measured based on 86Rb washout from cultured VMC in response to serum from SHR, Wistar-Kyoto rats (WKY), and Wistar rats (W). Serum from the three rat strains produced a substantial increase in the Ke of 86Rb washout from 9.6 +/- 1.7 for the control (C) of 17.3 +/- 2.0 for SHR. 15.3 +/- 0.9 for WKY, and 16.0 +/- 2.4 for W (x 10(-3)/min) (p less than 0.001 comparing C with SHR, W and p less than 0.01 comparing C with WKY respectively). However, comparison of the Ke of 86Rb washout among the three rats strains revealed no significant differences. It is concluded that serum increased passive K permeability of VSMC in culture. However, the data do not support the suggestion that some unknown humoral factors in the serum from SHR are involved in the abnormal alterations of membrane permeability to cations and thus contributing to the pathogenesis of hypertension in the SHR.

摘要

除了已知的影响自发性高血压大鼠(SHR)血管平滑肌细胞(VSMC)膜通透性的遗传异常外,血清体液因子可能在VSMC通透性改变中也起一定作用,并可能导致SHR高血压的发病机制。为了验证这一假设,根据从培养的VMC中86Rb洗脱的速率来测量被动钾通透性,该速率用洗脱速率常数(Ke)表示,以响应SHR、Wistar-Kyoto大鼠(WKY)和Wistar大鼠(W)的血清。三种大鼠品系的血清均使86Rb洗脱的Ke大幅增加,从对照组(C)的9.6±1.7增加到SHR的17.3±2.0、WKY的15.3±0.9和W的16.0±2.4(×10⁻³/min)(C与SHR、W相比,p<0.001;C与WKY相比,p<0.01)。然而,三种大鼠品系之间86Rb洗脱的Ke比较未发现显著差异。得出的结论是,血清增加了培养的VSMC的被动钾通透性。然而,数据并不支持以下观点:SHR血清中的某些未知体液因子参与了膜对阳离子通透性的异常改变,从而导致SHR高血压的发病机制。

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