摘要
目的研究大鼠阻力血管在α_１肾上腺素受体兴奋时内皮释放ＮＯ的变化。方法选用１６和４０周龄的自发性高血压大鼠（ＳＨＲ）和正常血压大鼠（ＷＫＹ）对照。用后肢阻力血管灌注模型来研究α_１肾上腺素受体兴奋剂（苯肾上腺素）的灌注压力曲线，以及在Ｌ－亚硝基精氨酸甲酯（ＬＮＡＭＥ）阻断ＮＯ的合成和用Ｌ－精氨酸（Ｌ－ａｒｇ）来增加ＮＯ合成的底物时，对苯肾上腺素的剂量反应曲线的影响。结果（ｌ）ＳＨＲ组ＰＰｍｉｎ，ＰＰｍａｘ，和Ｓｌｏｐｅ明显高于ＷＫＹ组，４０周ＥＣ_（５０）明显低于ＷＫＹ组，１６周时ＳＨＲ和ＷＫＹ没有明显差别。（２）ＳＨＲ后肢阻力血管对苯肾上腺素的反应明显强于ＷＫＹ组，用ＬＮＡＭＥ后苯肾上腺素的剂量反应曲线明显左移，用Ｌ－ａｒｇ后苯肾上腺素的剂量反应曲线在ＳＨＲ组没有明显变化．在ＷＫＹ组明显右移。结论（ｌ）α_１肾上腺素受体兴、奋时引起血管收缩的同时，引起内皮释放ＮＯ增加；（２）内皮释放ＮＯ在血管收缩时起负反馈的调节作用；（３）高血压时内皮细胞释放ＮＯ的功能障碍是导致阻力血管α_１肾上腺素受体兴奋剂反应性增加的原因之一。
To study the effect of endothelium releasing NO on the α1 adrenergic receptor excitement in resistant vessel in spontaneously hypertensive rats(SHR).Methods Spontaneously hypertensive rats and Wistar Kyoto rats, aged 16 and 40 weeks old,were used.The response of the hindquarter perfusion pressure to α1 adrenergic receptor agonist,phenylephrine,was studied,and in the absence or presence of Nω-nitro-L-arginine methyl ester(LNAME)and L-arginine(L-arg).Results PPmin,PPmax and slope were markedly higher in SHR than those of WKY,but in 16 wk of SHR no clifference was found from those of 40 wk of SHR. The reactivity of the hindquarter resistant vessel to phenylephrine was augmented as compared to WKY.In the presence of the LNAME,the responses to phenylephrine were enhanced in two groups rat.In the presence of L-arginine,the response was diminished only in WKY group ,however,in SHR group the response was similar to phenylephrine used alone. Conclusion These results suggested that the excitation of α1 adrenergic receptor not only induce the constriction of bloocl vessel,but also increase the release of NO from endothelium.The release of NO plays a feedback regulating role in the blood vessel constriction.The failure of releasing NO from endothelium may be a cause to lead the enhanced response to phenylephrine in SHR.
基金
福建省自然科学基金
