• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

原发性高血压中22钠流入红细胞的新方面。

New aspects concerning the 22sodium influx into red cells in essential hypertension.

作者信息

Wessels F, Zumkley H

出版信息

Klin Wochenschr. 1985;63 Suppl 3:38-41.

PMID:3999640
Abstract

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.

摘要

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。

相似文献

1
New aspects concerning the 22sodium influx into red cells in essential hypertension.原发性高血压中22钠流入红细胞的新方面。
Klin Wochenschr. 1985;63 Suppl 3:38-41.
2
The regulation of Na-K cotransport system and essential hypertension.钠钾协同转运系统与原发性高血压的调控
Klin Wochenschr. 1985;63 Suppl 3:52-4.
3
Altered erythrocyte cation transport related to hypertension or oral contraception.
Klin Wochenschr. 1985;63 Suppl 3:42-4.
4
Erythrocyte cation fluxes in essential hypertension of children and adolescents.
Int J Pediatr Nephrol. 1985 Jan-Mar;6(1):41-6.
5
Potassium influx into erythrocytes in essential hypertension.原发性高血压患者红细胞内钾离子流入情况
J Hypertens. 1984 Aug;2(4):405-9.
6
Vasoactive humoral systems and sodium transport in erythrocytes of normotensive offsprings of essential hypertensive subjects.
Physiol Bohemoslov. 1990;39(1):65-70.
7
[Evidence of abnormalities in net sodium and potassium fluxes in erythrocytes of patients with essential hypertension].[原发性高血压患者红细胞钠钾净通量异常的证据]
C R Seances Acad Sci D. 1979 Jan 29;288(4):453-5.
8
Low sodium cotransport in red cells with physiological internal sodium concentration in essential hypertension.原发性高血压患者红细胞中钠浓度正常时的低钠协同转运
Hypertension. 1984 Nov-Dec;6(6 Pt 1):826-31. doi: 10.1161/01.hyp.6.6.826.
9
Red cell Na+ -K+ transport in various forms of human hypertension. Role of cardiovascular risk factors and plasma potassium.各种类型人类高血压中的红细胞钠钾转运。心血管危险因素和血钾的作用。
Klin Wochenschr. 1985;63 Suppl 3:63-5.
10
Erythrocyte Na+-K+ cotransport in elderly hypertensive subjects.老年高血压患者的红细胞钠钾协同转运
Isr J Med Sci. 1985 Mar;21(3):314-6.

引用本文的文献

1
Abnormal erythrocyte sodium leak in a subset of essential hypertensive patients.
Klin Wochenschr. 1989 Jan 4;67(1):31-7.