Salardi S, Modica R, Ferrandi M, Ferrari P, Torielli L, Bianchi G
Istituto Ricerche Farmitalia-Carlo Erba, Nerviano, Milan, Italy.
J Hypertens Suppl. 1988 Dec;6(4):S196-8. doi: 10.1097/00004872-198812040-00058.
Previous studies showed that erythrocytes from the Milan hypertensive strain of rats (MHS) are smaller and have a faster Na-K cotransport when compared with their normotensive controls (MNS). These characteristics are determined within the stem cell, are genetically associated with hypertension and are similar to other renal tubular cell abnormalities more directly involved in the development of hypertension in MHS. The difference in volume is maintained in ghost membranes, while the difference in transport is abolished in inside-out vesicles. Ghosts and cytoskeletons contain a 105-kilodalton protein already characterized by immunoblotting. This protein has been identified with erythrocyte adducin by several criteria, including binding to calmodulin and protein kinase C, phosphorylation and full immunological cross-reactivity with human adducin. Since only MHS rats immunized with MNS erythrocyte cytoskeletons produce anti-adducin antibodies, we suggest an immunogenic structural difference in adducin from the two strains, and an involvement of this difference in the alteration of Na-K cotransport observed.
先前的研究表明，与正常血压对照大鼠（MNS）相比，米兰高血压大鼠品系（MHS）的红细胞较小，且钠钾协同转运更快。这些特征在干细胞内就已确定，与高血压存在遗传关联，并且类似于其他更直接参与MHS高血压发生发展的肾小管细胞异常。在血影膜中体积差异得以维持，而在内外翻转囊泡中转运差异则消失。血影和细胞骨架含有一种已通过免疫印迹法鉴定的105千道尔顿蛋白。通过包括与钙调蛋白和蛋白激酶C结合、磷酸化以及与人内收蛋白完全免疫交叉反应等多项标准，该蛋白已被鉴定为红细胞内收蛋白。由于只有用MNS红细胞细胞骨架免疫的MHS大鼠产生抗内收蛋白抗体，我们推测这两个品系的内收蛋白存在免疫原性结构差异，且这种差异参与了所观察到的钠钾协同转运改变。
