摘要
本实验旨在观察肾动脉内注射ＥＴ－１对麻醉大鼠血压（ＢＰ）、心率（ＨＲ）和肾神经传入放电（ＡＲＮＡ）的影响，以及ＥＴＡ受体阻断剂ＢＱ－１２３和硝苯吡啶（Ｎｉｆ）对ＥＴ生物学效应的拮抗作用。结果如下：（１）肾动脉注射ＥＴ－１（１μｇ／ｋｇ）后，平均动脉压（ＭＡＰ）先有短暂的降低（由１３．７７±０．１３ｋＰａ降至１０．２±１．１２ｋＰａ），随后为较显著的持久增高，增值达３．４４±１．６０ｋＰａＰ＜０．００１），ＨＲ无明显变化，ＡＲＮＡ增加１０８．３３±１６．６７％（Ｐ＜０．００１）。（２）肾动脉内注射ＥＴＡ受体选择性拮抗剂ＢＱ－１２３（１５０μｇ／ｋｇ），ＥＴ－１的上述效应即被拮抗。与ＥＴ组相比差异非常显著（Ｐ＜０．００１）。（３）肾动脉内注射二氢吡啶敏感性Ｌ－型钙通道阻断剂Ｎｉｆ（０．１ｍｇ／ｋｇ），也可明显抑制ＥＴ－１的上述效应，与ＥＴ组相比差异十分显著（Ｐ＜０．００１）。以上结果表明：肾动脉内注射ＥＴ－１引起的麻醉大鼠ＭＡＰ增高和ＡＲＮＡ积分增加的作用，可能是由ＥＴＡ受体介导的。
he present investigation was carried out in anesthetized rat to observe the effects of intrarenal arterial injection of endothelin-1 (ET-1) on mean arterial pressure (MAP), heart rate (HR) and afferent renal nerve activity (ARNA), and to examine the antagonistic effects of a selective (ETA) receptor antagonist. BQ123 and nifedipine (Nif) on the biological actions of ET-1. The results obtained were as follows: (1) In response to intrarenal arterial injection of ET1 (1 μg/kg) MAP was initially decreased (from 13.77±0.13 to 10. 2±1.12 kPa) and subsequently increased (from 13.77±0.13 to 17. 21±1.73 kPa, P<0.001), and ARNA was increased by 108. 33±16. 67% (P<0.001), while HR showed no significant change. (2) Pretreatment with a selective ETA receptor antagonist BQ123 (150 μg/kg) could effectively antagonize the above biological actions induced by ET-1. (3) The dihydropyridine sensitive L-type calcium channel blocker Nif (0.1 mg/kg) administered by intrarenal arterial route could also block the biological actions of ET-1. From the results, it is suggested that the increases in MAP and ARNA induced by intrarenal arterial injection ET-1 may be mediated by ET-A receptors, and the cellular mechanism underlying the actions of ET-1 may be attributed to an intracellular calciumoverload.
出处
《中国应用生理学杂志》
CAS
CSCD
1998年第3期254-257,共4页
Chinese Journal of Applied Physiology
基金
河北省自然科学基金
