• 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

Kinetic study of Na+-K+ pump in erythrocytes from essential hypertensive patients.

作者信息

Diez J, Hannaert P, Garay R P

出版信息

Am J Physiol. 1987 Jan;252(1 Pt 2):H1-6. doi: 10.1152/ajpheart.1987.252.1.H1.

DOI:10.1152/ajpheart.1987.252.1.H1
PMID:3028158
Abstract

The interaction of the Na+-K+ pump with internal Na+ was investigated in erythrocytes from 38 normotensive control subjects and 49 essential hypertensive patients. In six of the hypertensive patients, the Na+-K+ pump exhibited an apparent dissociation constant for internal Na+ (KNa) above an upper normal limit of 7 mmol/l cells. Four of these six hypertensives showed an increase in the maximal rate of ouabain-sensitive Na+ efflux (Vmax), above an upper normal limit of 11 mmol X l cells-1 X h-1. These abnormalities were stable in repeated determinations over 1-3 yr. A kinetic study of other erythrocyte Na+ transport pathways showed that 16 hypertensives had a low apparent affinity of the Na+-K+ cotransport system for internal Na+, 10 hypertensives exhibited increased Na+-Li+ countertransport fluxes, and 11 hypertensives had increased Na+ leak. None of these three abnormalities were observed in the six hypertensives with abnormal pump fluxes. We thus propose to denominate them as Pump (-) hypertensives. Interestingly, four Pump (-) hypertensives exhibited an increased maximal rate of outward Na+-K+ cotransport. Basal erythrocyte Na+ content of Pump (-) hypertensives was within normal range. This suggests that the increased maximal rates of the Na+-K+ pump and Na+-K+ cotransport system compensate the low pump affinity for internal Na+.

摘要

相似文献

1
Kinetic study of Na+-K+ pump in erythrocytes from essential hypertensive patients.
Am J Physiol. 1987 Jan;252(1 Pt 2):H1-6. doi: 10.1152/ajpheart.1987.252.1.H1.
2
Abnormal Na+-K+ ATPase kinetics in a subset of essential hypertensive patients.
Eur J Clin Invest. 1988 Aug;18(4):337-42. doi: 10.1111/j.1365-2362.1988.tb01021.x.
3
A classification of essential hypertensive patients according to the erythrocyte Na transport abnormalities: an application for monitoring the antihypertensive response to cicletanide.根据红细胞钠转运异常对原发性高血压患者进行分类:应用于监测环戊噻嗪的降压反应。
Klin Wochenschr. 1985;63 Suppl 3:30-2.
4
Abnormal erythrocyte sodium leak in a subset of essential hypertensive patients.
Klin Wochenschr. 1989 Jan 4;67(1):31-7.
5
Outward Na+-K+-Cl- cotransport function in erythrocytes from essential hypertensives.原发性高血压患者红细胞外向钠-钾-氯协同转运功能
J Hum Hypertens. 1989 Feb;3(1):1-8.
6
Na+ leak in erythrocytes from essential hypertensive patients.
Clin Sci (Lond). 1985 Nov;69(5):613-24. doi: 10.1042/cs0690613.
7
Cation fluxes and Na+-K+-activated ATPase activity in erythrocytes of patients with essential hypertension.
Hypertension. 1981 Nov-Dec;3(6):641-9. doi: 10.1161/01.hyp.3.6.641.
8
Red cell lithium-sodium countertransport and sodium-potassium cotransport in patients with essential hypertension.原发性高血压患者的红细胞锂-钠逆向转运和钠-钾协同转运
Hypertension. 1982 Nov-Dec;4(6):795-804. doi: 10.1161/01.hyp.4.6.795.
9
Na-K-adenosine triphosphatase and cation content in the erythrocyte in essential hypertension.原发性高血压患者红细胞中的钠钾三磷酸腺苷酶及阳离子含量
J Lab Clin Med. 1986 Apr;107(4):337-41.
10
Inherited defect in a Na+, K-co-transport system in erythrocytes from essential hypertensive patients.原发性高血压患者红细胞中钠钾协同转运系统的遗传性缺陷。
Nature. 1980 Mar 20;284(5753):281-3. doi: 10.1038/284281a0.

引用本文的文献

1
A Computer Model of Oxygen Dynamics in the Cortex of the Rat Kidney at the Cell-Tissue Level.大鼠肾皮质细胞-组织水平氧动力学的计算机模型。
Int J Mol Sci. 2019 Dec 11;20(24):6246. doi: 10.3390/ijms20246246.
2
Abnormal erythrocyte sodium leak in a subset of essential hypertensive patients.
Klin Wochenschr. 1989 Jan 4;67(1):31-7.