• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Endogenous endothelin attenuates the pressor response to acute environmental stress via the ETA receptor.
【24h】

Endogenous endothelin attenuates the pressor response to acute environmental stress via the ETA receptor.

机译：内源性内皮素通过ETA受体减弱了对急性环境压力的升压反应。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Clinical studies have documented an abrupt rise in plasma endothelin-1 (ET-1) coincident with an increase in mean arterial pressure (MAP) during the response to acute stress. We therefore examined the ET(A) and ET(B) receptor-dependent effects of ET-1 on the pressor response to acute environmental stress in ET-1-dependent hypertension. Stress was induced by administration of air jet pulses (3 min) in ET(B) receptor-deficient (ET(B) sl/sl) rats fed normal salt (NS; 0.8% NaCl), high salt (HS; 8% NaCl), and HS plus the ET(A) receptor antagonist ABT-627 (5 mg.kg(-1).day(-1)) on successive weeks. MAP was chronically monitored by telemetry. Total pressor response (area under the curve) was significantly reduced in ET(B) sl/sl rats maintained on a HS vs. NS diet [-6.8 mmHg (SD 18.7) vs. 29.3 mmHg (SD 8.1) x 3 min, P < 0.05]. Conversely, the total pressor response was augmented in both wild-type [34.2 mmHg (SD 29.2) x 3 min, P < 0.05 vs. NS] and ET(B) sl/sl rats [49.1 mmHg (SD 11.8) x 3 min, P < 0.05 vs. NS] by ABT-627. Blockade of ET(B) receptors in Sprague-Dawley rats caused an increase in basal MAP that was enhanced by HS and lowered by mixed ET(A)/ET(B) receptor antagonism; none of these treatments, however, had any effect on the pressor response. These data demonstrate that increasing endogenous ET-1 suppresses the pressor response to acute stress through ET(A) receptor activation in a genetic model of ET-1-dependent hypertension. These results are consistent with reports that ET-1 can attenuate sympathetically mediated responses.
机译：临床研究表明，血浆内皮素-1（ET-1）的突然升高与急性应激反应期间平均动脉压（MAP）的升高同时发生。因此，我们研究了ET-1依赖性高血压中ET-1对急性环境应激的升压反应的ET（A）和ET（B）受体依赖性作用。在饲喂普通盐（NS; 0.8％NaCl），高盐（HS; 8％NaCl）的ET（B）受体缺乏症（ET（B）sl / sl）大鼠中，通过施加空气喷射脉冲（3分钟）诱导了应激。 ），HS以及连续几周的ET（A）受体拮抗剂ABT-627（5 mg.kg（-1）.day（-1））。通过遥测对MAP进行了长期监控。维持HS和NS饮食的ET（B）sl / sl大鼠的总升压反应（曲线下的面积）显着降低[-6.8 mmHg（SD 18.7）vs. 29.3 mmHg（SD 8.1）x 3分钟，P <0.05]。相反，野生型[34.2 mmHg（SD 29.2）x 3分钟，P <0.05 vs. NS]和ET（B）sl / sl大鼠[49.1 mmHg（SD 11.8）x 3 min ，相对于NS，P <0.05]。 Sprague-Dawley大鼠体内对ET（B）受体的阻断导致基础MAP的增加，HS增强了基础MAP的作用，而ET（A）/ ET（B）混合受体拮抗作用降低了基础MAP的水平。然而，这些处理均未对升压反应产生任何影响。这些数据表明，在依赖ET-1的高血压遗传模型中，内源性ET-1的增加会抑制ET（A）受体激活引起的对急性应激的升压反应。这些结果与ET-1可以减弱交感介导的反应的报道一致。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号