Uchiyama M
Department of Pediatrics, Oita Medical University.
Nihon Jinzo Gakkai Shi. 1992 Sep;34(9):1025-9.
The number of sodium pump receptors in erythrocytes (maximum binding of ouabain to erythrocytes; Bmax) was examined in relation to a family history of essential hypertension (FH-HT), the body mass index (BMI), urinary sodium excretion and blood pressure in 71 normotensive children (13 to 15 years of age), and in relation to sodium intake in 6 children who had various kidney diseases but displayed a normal renal function (6 to 13 years of age). Bmax was significantly lower in children with FH-HT than in those without FH-HT. However, the BMI, urinary sodium excretion and blood pressure showed no significant differences between the groups. Bmax was not significantly different between the top 20% tile group of BMI or urinary sodium excretion and the bottom 20% tile group of BMI or urinary sodium excretion. Furthermore, Bmax was unchanged during and after restriction of sodium intake in children with nephropathy. These findings suggest that Bmax may be a genetic marker for essential hypertension, since it was suppressed regardless of the BMI or urinary sodium excretion in normotensive children with FH-HT, and since it did not change according to sodium intake in children with renal diseases.
在71名血压正常的儿童(13至15岁)中,研究了红细胞中钠泵受体的数量(哇巴因与红细胞的最大结合量;Bmax)与原发性高血压家族史(FH-HT)、体重指数(BMI)、尿钠排泄及血压的关系;在6名患有各种肾脏疾病但肾功能正常的儿童(6至13岁)中,研究了Bmax与钠摄入量的关系。有FH-HT的儿童的Bmax显著低于无FH-HT的儿童。然而,两组之间的BMI、尿钠排泄及血压无显著差异。BMI或尿钠排泄前20%组与BMI或尿钠排泄后20%组之间的Bmax无显著差异。此外,肾病患儿在限制钠摄入期间及之后Bmax无变化。这些发现表明,Bmax可能是原发性高血压的一个遗传标志物,因为在有FH-HT的血压正常儿童中,无论BMI或尿钠排泄情况如何,Bmax均受到抑制,且在肾病患儿中,Bmax不随钠摄入量的变化而改变。