Poston L, Sewell R B, Wilkinson S P, Richardson P J, Williams R, Clarkson E M, MacGregor G A, de Wardener H E
Br Med J (Clin Res Ed). 1981 Mar 14;282(6267):847-9. doi: 10.1136/bmj.282.6267.847.
The active sodium transport of white cells and red cells obtained from patients with essential hypertension was impaired. Incubating white cells from normotensive subjects in serum obtained from patients with essential hypertension caused an impairment in sodium transport in the white cells of normotensive subjects similar to that found in the white cells of hypertensive patients. The impairment in sodium transport was due to a fall in the ouabain-sensitive component of the total sodium efflux rate constant. These results show that the serum of patients with essential hypertension contains a substance which influences sodium transport and that it has ouabain-like activity. They also suggest that it is this substance which causes the impairment in sodium transport in the leucocytes of patients with essential hypertension. These findings support the hypothesis that the rise in blood pressure in patients with essential hypertension is due to an increased concentration of a circulating sodium transport inhibitor which is continuously correcting a tendency for sodium retention by the kidney.
原发性高血压患者的白细胞和红细胞的主动钠转运受损。将血压正常者的白细胞置于原发性高血压患者的血清中孵育,会导致血压正常者白细胞的钠转运受损,类似于高血压患者白细胞中的情况。钠转运受损是由于总钠外流速率常数中哇巴因敏感成分下降所致。这些结果表明,原发性高血压患者的血清中含有一种影响钠转运的物质,且具有类似哇巴因的活性。它们还提示,正是这种物质导致原发性高血压患者白细胞的钠转运受损。这些发现支持了这样一种假说,即原发性高血压患者血压升高是由于循环中钠转运抑制剂浓度增加,该抑制剂持续纠正肾脏钠潴留的倾向。