Brod J, Schaeffer J, Hengstenberg J H, Kleinschmidt T G
Clin Sci (Lond). 1984 Mar;66(3):351-5. doi: 10.1042/cs0660351.
The ouabain-sensitive 42K+ flux from an artificial medium into erythrocytes was measured in 29 control subjects, 66 patients with chronic parenchymatous renal disease and in 32 subjects with primary hypertension. The ouabain-sensitive 42K+ influx was reduced in subjects with chronic renal disease by about 20%, even when they were normotensive. The reduction in these patients was greater than that in patients with essential hypertension. The changes in 42K+ influx and Na+ content with a decrease in the 42K+ influx/Na+ content ratio suggest an inhibition of the Na+ pump in the patients with chronic renal disease. The inhibition of the Na+ pump may be secondary to the hypervolaemia which we suggest is the initial event leading to renal hypertension.
在29名对照受试者、66名慢性实质性肾病患者和32名原发性高血压患者中,测量了哇巴因敏感的42K⁺从人工培养基进入红细胞的通量。慢性肾病患者中,即使血压正常,哇巴因敏感的42K⁺内流也减少了约20%。这些患者的减少幅度大于原发性高血压患者。随着42K⁺内流和Na⁺含量的变化,42K⁺内流/Na⁺含量比值降低,提示慢性肾病患者的Na⁺泵受到抑制。Na⁺泵的抑制可能继发于血容量过多,我们认为这是导致肾性高血压的初始事件。