Wessels F, Zumkley H
Klin Wochenschr. 1985;63 Suppl 3:38-41.
The different components of the total 22Na influx into red cells (RC) of 21 normotensive subjects and 38 patients with essential hypertension were measured and correlated together. We found that the acceleration of total net 22Na influx in essential hypertension is predominantly caused by an increase of the Na leak and only in a small part effected by an elevated phloretin-sensitive Na countertransport. The 22Na influx mediated by the anion exchange system and the furosemide inhibitable Na-K cotransport were not significantly altered. The correlations suggest that the total 22Na influx into RC of normotensive subjects is very strong and equally defined by both the Na leak and the anion exchange system, whereas an influence of the Na countertransport is not detectable. On the contrary we found a clear decreased dependence upon the anion exchange system in favour of the countertransport in patients with essential hypertension, while the influence of Na leak was unaltered.
对21名血压正常受试者和38名原发性高血压患者红细胞(RC)中22Na总内流的不同组成部分进行了测量,并将它们相互关联。我们发现,原发性高血压中总净22Na内流的加速主要是由钠泄漏增加引起的,只有一小部分受根皮素敏感的钠逆向转运升高的影响。由阴离子交换系统介导的22Na内流和呋塞米可抑制的钠钾协同转运没有显著改变。相关性表明,血压正常受试者红细胞中22Na总内流非常强烈,并且由钠泄漏和阴离子交换系统共同明确界定,而钠逆向转运的影响无法检测到。相反,我们发现原发性高血压患者对阴离子交换系统的依赖性明显降低,有利于逆向转运,而钠泄漏的影响未改变。