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自发性高血压大鼠红细胞钙处理的改变。高血压状态下钙诱导的红细胞渗透脆性变化。

Alterations in calcium-handling of erythrocytes in spontaneously hypertensive rats. Calcium-induced changes in the osmotic fragility of erythrocytes in hypertension.

作者信息

Tsuda K, Minatogawa Y, Tsuda S, Shima H, Nishio I, Kido R, Masuyama Y

机构信息

Department of Medicine, Wakayama Medical College, Japan.

出版信息

Jpn Heart J. 1987 Nov;28(6):923-31. doi: 10.1536/ihj.28.923.

Abstract

To investigate the sensitivity to calcium of erythrocytes in hypertension, changes in the osmotic fragility of erythrocytes following Ca-loading were observed. Washed erythrocytes were obtained from spontaneously hypertensive rats (SHR, Okamoto and Aoki) and age-matched normotensive Wistar Kyoto rats (WKY). Treatment of erythrocytes with Ca-ionophore A23187 and Ca in the medium caused a reduction in the osmotic fragility which correlated with the Ca-concentration. The degree of alteration in the osmotic fragility of erythrocytes was greater in SHR than in WKY. Oral administration of hydralazine to SHR significantly reduced the blood pressure. However, the alterations in the osmotic fragility of erythrocytes secondary to Ca-loading were not different between hydralazine-treated and untreated SHR. In the presence of a Ca-antagonist (verapamil or diltiazem) in the medium, the reduction of the osmotic fragility of erythrocytes caused by Ca-loading was inhibited, and the differences between SHR and WKY were abolished by Ca-antagonists. These results suggest that the greater changes in osmotic fragility of erythrocytes caused by Ca-loading in SHR could be due to a genetic abnormality of Ca-handling by the cell membranes, and that this abnormality might cause an increase in intracellular Ca, which contributes, in part, to the pathogenesis of hypertension.

摘要

为研究高血压患者红细胞对钙的敏感性,观察了钙负荷后红细胞渗透脆性的变化。从自发性高血压大鼠(SHR,冈本和青木品系)和年龄匹配的正常血压Wistar Kyoto大鼠(WKY)获取洗涤后的红细胞。用钙离子载体A23187和培养基中的钙处理红细胞会导致渗透脆性降低,且这种降低与钙浓度相关。SHR红细胞渗透脆性的改变程度大于WKY。给SHR口服肼屈嗪可显著降低血压。然而,肼屈嗪治疗组和未治疗组的SHR在钙负荷后红细胞渗透脆性的改变并无差异。在培养基中存在钙拮抗剂(维拉帕米或地尔硫䓬)时,钙负荷引起的红细胞渗透脆性降低受到抑制,且钙拮抗剂消除了SHR和WKY之间的差异。这些结果表明,SHR中钙负荷导致的红细胞渗透脆性更大变化可能归因于细胞膜钙处理的遗传异常,并且这种异常可能导致细胞内钙增加,这在一定程度上促成了高血压的发病机制。

相似文献

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Erythrocyte membrane abnormalities in hypertension: a comparison between two animal models.
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