• 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

对盐诱导高血压敏感或耐受的 Dahl 大鼠肺血管去甲肾上腺素的流出量

Pulmonary vascular efflux of norepinephrine in Dahl rats susceptible or resistant to salt-induced hypertension.

作者信息

Metting P J, Duggan J M

机构信息

Department of Physiology, Medical College of Ohio, Toledo 43699.

出版信息

Proc Soc Exp Biol Med. 1988 Jun;188(2):212-8. doi: 10.3181/00379727-188-42730.

DOI:10.3181/00379727-188-42730
PMID:3375267
Abstract

The purpose of these studies was to determine whether the accumulation of norepinephrine by the pulmonary circulation is altered in the Dahl model of genetic hypertension. Pulmonary norepinephrine accumulation was evaluated by performing a compartmental analysis of the efflux of L-[3H]norepinephrine from perfused lungs after inhibition of the norepinephrine-metabolizing enzymes. The lungs were isolated from Dahl salt-hypertension-susceptible (S) and salt-hypertension-resistant (R) rats that had been on a high sodium diet for 3 weeks. In both S and R rats, norepinephrine was accumulated into a single compartment with an efflux half-time of approximately 23 min, in addition to its distribution in the extracellular space. The size of the extracellular space was significantly increased in the S rats, but there was no difference in the size of the compartment of L-[3H]norepinephrine efflux between S (6.4 +/- 1.2 ml/g) and R (3.7 +/- 0.7 ml/g) rats. These data indicate that impaired accumulation and efflux of norepinephrine by the lungs does not contribute to the pathogenesis of hypertension in Dahl S rats.

摘要

这些研究的目的是确定在遗传性高血压的 Dahl 模型中,肺循环中去甲肾上腺素的蓄积是否发生改变。通过在抑制去甲肾上腺素代谢酶后,对灌注肺中 L-[3H]去甲肾上腺素的流出进行房室分析,来评估肺去甲肾上腺素的蓄积情况。从食用高钠饮食 3 周的 Dahl 盐敏感性高血压(S)大鼠和盐抵抗性高血压(R)大鼠中分离出肺。在 S 大鼠和 R 大鼠中,除了去甲肾上腺素在细胞外空间的分布外,它还蓄积到一个单一房室中,流出半衰期约为 23 分钟。S 大鼠的细胞外空间大小显著增加,但 S 大鼠(6.4±1.2 ml/g)和 R 大鼠(3.7±0.7 ml/g)之间 L-[3H]去甲肾上腺素流出房室的大小没有差异。这些数据表明,肺对去甲肾上腺素的蓄积和流出受损并不促成 Dahl S 大鼠高血压的发病机制。

相似文献

1
Pulmonary vascular efflux of norepinephrine in Dahl rats susceptible or resistant to salt-induced hypertension.对盐诱导高血压敏感或耐受的 Dahl 大鼠肺血管去甲肾上腺素的流出量
Proc Soc Exp Biol Med. 1988 Jun;188(2):212-8. doi: 10.3181/00379727-188-42730.
2
Compartmental analysis of the efflux of l-[3H]norepinephrine from isolated perfused rat lungs.对从离体灌注大鼠肺中流出的 l-[3H]去甲肾上腺素进行的房室分析。
J Appl Physiol (1985). 1985 Jan;58(1):244-50. doi: 10.1152/jappl.1985.58.1.244.
3
3H-norepinephrine release in hypothalamus and brainstem of Dahl-salt sensitive and resistant rats in vitro.
Clin Exp Hypertens A. 1986;8(8):1395-411. doi: 10.3109/10641968609044094.
4
Characterization of new inbred strains of Dahl-Iwai salt-sensitive and salt-resistant rats.新型Dahl-Iwai盐敏感和盐抵抗大鼠近交系的特性分析
Lab Anim Sci. 1994 Oct;44(5):462-7.
5
Sustained hypertension in Dahl rats. Negative correlation of agonist response to blood pressure.
Hypertension. 1995 Jan;25(1):139-45. doi: 10.1161/01.hyp.25.1.139.
6
Dahl salt-sensitive rats and human essential hypertension.Dahl盐敏感大鼠与人类原发性高血压
J Hypertens Suppl. 1986 Oct;4(3):S29-31.
7
Vitamin E ameliorates the renal injury of Dahl salt-sensitive rats.维生素E可改善 Dahl 盐敏感大鼠的肾损伤。
Am J Hypertens. 1997 May;10(5 Pt 2):116S-119S.
8
Renal P450 metabolites of arachidonic acid and the development of hypertension in Dahl salt-sensitive rats.花生四烯酸的肾脏P450代谢产物与Dahl盐敏感大鼠高血压的发生
Am J Hypertens. 1997 May;10(5 Pt 2):63S-67S.
9
Catecholamine and neuropeptide Y levels in tissues from young Dahl rats following 5 days low- or high-salt diet.5天低钠或高钠饮食后年轻Dahl大鼠组织中的儿茶酚胺和神经肽Y水平
Blood Vessels. 1991;28(6):442-51. doi: 10.1159/000158891.
10
AT(1) receptor regulation in salt-sensitive hypertension.盐敏感性高血压中血管紧张素Ⅱ1型受体的调节
Am J Physiol. 1999 Nov;277(5):H1701-7. doi: 10.1152/ajpheart.1999.277.5.H1701.