Yoon Y S, Bang B K, Min B S, Kim H J
Korean J Intern Med. 1986 Jul;1(2):185-93. doi: 10.3904/kjim.1986.1.2.185.
To study the relationship between natriuretic factor and experimental low renin hypertension, the erythrocyte Na-K ATPase activities in the genesis of reducing renal mass in hypertensive rats were measured. The results were as follows : 1. The fractional excretion of Na in hypertensive, reduced renal mass rats (saline-drinking) was higher than that of normotensive, reduced renal mass rats (water-drinking) (p<.001). The plasma renin activities in the hypertensive group were markedly lower than those of the normotensive group (p<.001). 2. The total ATPase activities of rat erythrocyte membrane in the hypertensive group were lower than in those of the normal and the normotensive groups (p<.001, p<.02). 3. The Mg-ATPase activities of rat erythrocyte membrane in the normotensive group tended to decrease significantly (p<.001), but the differences between the normotensive and hypertensive group were not significant. 4. The Na-K ATPase activities of rat erythrocyte membrane in the hypertensive group were lower than those of the normal and the normotensive group (p<.001). However, the difference between the normal and the normotensive groups was not significant. 5. When erythrocyte membrane taken from normal rats was incubated with supernates of boiled plasma from normotensive rats, the total ATPase activities of erythrocyte membrane were not different from those of hypertensive rats. 6. When erythrocyte membrane taken from normal rats was incubated with supernates of boiled plasma from normotensive rats, the Mg ATPase activities of erythrocyte membrane were lower than those of hypertensive rats (p<.01). 7. When erythrocyte membrane taken from normal rats was incubated with supernates of boiled plasma from hypertensive rats, the Na-K ATPase activities of erythrocyte membrane were lower than those of normotensive rats (p<.01). Based on the above findings, it is suggested that the pathogenesis of low renin, reduced renal mass hypertension is primarily mediated by a natriuretic factor (or an ouabain-like factor, inhibitor of Na-K ATPase) produced by extracellular fluid volume expansion.
为研究利钠因子与实验性低肾素性高血压之间的关系，测定了高血压大鼠肾质量减少发生过程中红细胞钠钾ATP酶活性。结果如下：1. 高血压、肾质量减少大鼠（饮用盐水）的钠分数排泄高于正常血压、肾质量减少大鼠（饮用纯水）（p<0.001）。高血压组的血浆肾素活性明显低于正常血压组（p<0.001）。2. 高血压组大鼠红细胞膜的总ATP酶活性低于正常组和正常血压组（p<0.001，p<0.02）。3. 正常血压组大鼠红细胞膜的镁ATP酶活性有显著降低趋势（p<0.001），但正常血压组与高血压组之间差异不显著。4. 高血压组大鼠红细胞膜的钠钾ATP酶活性低于正常组和正常血压组（p<0.001）。然而，正常组与正常血压组之间差异不显著。5. 当将正常大鼠的红细胞膜与正常血压大鼠煮沸血浆的上清液一起孵育时，红细胞膜的总ATP酶活性与高血压大鼠的无差异。6. 当将正常大鼠的红细胞膜与正常血压大鼠煮沸血浆的上清液一起孵育时，红细胞膜的镁ATP酶活性低于高血压大鼠（p<0.01）。7. 当将正常大鼠的红细胞膜与高血压大鼠煮沸血浆的上清液一起孵育时，红细胞膜的钠钾ATP酶活性低于正常血压大鼠（p<0.01）。基于上述发现，提示低肾素、肾质量减少性高血压的发病机制主要由细胞外液量扩张产生的利钠因子（或哇巴因样因子，钠钾ATP酶抑制剂）介导。
