• 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

视前区慢性损伤对大鼠肾脏钠排泄的影响。

Effect of chronic preoptic lesions on the renal excretion of sodium in rats.

作者信息

Keeler R

出版信息

Am J Physiol. 1975 Jun;228(6):1725-8. doi: 10.1152/ajplegacy.1975.228.6.1725.

DOI:10.1152/ajplegacy.1975.228.6.1725
PMID:1155604
Abstract

Rats with bilateral lesions in the preoptic area showed a normal pattern of urineand electrolyte excretion under resting conditions but complete absence of a natriuretic response to unilateral carotid baroreceptor stimulation and also a significant reduction in the rate of sodium excretion after saline loading and after a high-sodium intake. Measurements of renal clearance did not show any significant differences in glomerular filtration rate, renal plasma flow, or filtration fraction between normal and preoptic-lesion rats. Apart from the test situations used above, rats with preoptic lesions were apparently able to regulate their sodium metabolism normally because after 3 wk on a high-sodium intake their plasma and extracellular fluid volumes, plasma electrolytes, osmolaity, and mean arterial pressures were indistinguishable from normal rats. It is suggested that the preoptic component of the baroreceptor reflex pathway mighthave an input into a hypothalamic area controlling sodium excretion.

摘要

视前区双侧受损的大鼠在静息状态下尿液和电解质排泄模式正常,但对单侧颈动脉压力感受器刺激完全没有利钠反应,并且在生理盐水负荷后和高钠摄入后钠排泄率也显著降低。肾清除率测量结果显示,正常大鼠和视前区受损大鼠之间的肾小球滤过率、肾血浆流量或滤过分数没有任何显著差异。除了上述测试情况外,视前区受损的大鼠显然能够正常调节其钠代谢,因为在高钠摄入3周后,它们的血浆和细胞外液体积、血浆电解质、渗透压和平均动脉压与正常大鼠没有区别。有人认为,压力感受器反射通路的视前区成分可能会向控制钠排泄的下丘脑区域输入信号。

相似文献

1
Effect of chronic preoptic lesions on the renal excretion of sodium in rats.视前区慢性损伤对大鼠肾脏钠排泄的影响。
Am J Physiol. 1975 Jun;228(6):1725-8. doi: 10.1152/ajplegacy.1975.228.6.1725.
2
Dependence of saline-induced natriuresis upon exposure of the kidney to the physical effects of extracellular fluid volume expansion.盐诱导的利钠作用对肾脏暴露于细胞外液容量扩张的物理效应的依赖性。
J Clin Invest. 1974 Dec;54(6):1428-36. doi: 10.1172/JCI107890.
3
Preoptic-hypothalamic periventricular lesions reduce natriuresis to volume expansion.视前区-下丘脑室周病变会降低因容量扩张引起的利钠作用。
Am J Physiol. 1983 Jan;244(1):R51-7. doi: 10.1152/ajpregu.1983.244.1.R51.
4
Demonstraton of a role of physical factors as determinants of the natriuretic response to volume expansion.证明物理因素作为容量扩张钠利尿反应决定因素的作用。
J Clin Invest. 1967 Dec;46(12):1963-78. doi: 10.1172/JCI105686.
5
Effects of hematocrit on renal hemodynamics and sodium excretion in hydropenic and volume-expanded dogs.血细胞比容对禁水和血容量增加犬的肾血流动力学及钠排泄的影响。
J Clin Invest. 1970 Sep;49(9):1656-67. doi: 10.1172/JCI106383.
6
Modification of carotid chemoreceptor-induced changes in renal haemodynamics and function by carotid baroreflex in dogs.犬颈动脉压力反射对颈动脉化学感受器引起的肾血流动力学和功能变化的调节作用
J Physiol. 1993 Jul;466:599-610.
7
Studies on the exaggerated natriuretic response to a saline infusion in the hypothyroid rat.甲状腺功能减退大鼠对生理盐水输注的利钠反应增强的研究。
J Clin Invest. 1970 Jun;49(6):1224-36. doi: 10.1172/JCI106336.
8
[Renal function in changes in the volume and composition of the extracellular fluid].[细胞外液容量与成分变化时的肾功能]
Usp Fiziol Nauk. 1986 Jan-Mar;17(1):77-91.
9
The effect of Ringer solution induced extracellular volume expansion on kidney function.林格液诱导的细胞外液容量扩张对肾功能的影响。
Acta Physiol Hung. 1989;74(2):141-60.
10
Effect of lateral hypothalamus lesions on the water and salt intake, and sodium and urine excretion induced by activation of the median preoptic nucleus in conscious rats.外侧下丘脑损伤对清醒大鼠中视前核激活诱导的水盐摄入及钠和尿排泄的影响。
J Auton Nerv Syst. 1995 Jun 25;53(2-3):195-204. doi: 10.1016/0165-1838(94)00176-k.

引用本文的文献

1
Natriuretic hormones, endogenous ouabain, and related sodium transport inhibitors.利钠激素、内源性哇巴因及相关钠转运抑制剂。
Front Endocrinol (Lausanne). 2014 Dec 3;5:199. doi: 10.3389/fendo.2014.00199. eCollection 2014.