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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。
OBJECTIVE: To study the changes of nitric oxide (NO) released from endothelial cells during the activation of α 1 adrenoceptors in rat resistance blood vessels. Methods Spontaneous hypertensive rats (SHR) and normotensive rats (WKY) at 16 and 40 weeks of age were selected. The hindlimb resistance vascular perfusion model was used to study the perfusion pressure curve of the alpha 1 adrenergic receptor agonist (phenylephrine) and the synthesis of NO blocked with L-nitroso-arginine methyl ester (LNAME) (L-arg) to increase the NO synthesis of the substrate on the phenylephrine dose-response curve. Results (1) The PPmin, PPmax and Slope in SHR group were significantly higher than those in WKY group. The EC 50 in 40 weeks was significantly lower than that in WKY group. There was no significant difference between SHR and WKY at 16 weeks. (2) SHR hindlimb resistance blood vessels response to phenylephrine was significantly stronger than WKY group, with LNAME after phenylephrine dose response curve was significantly shifted to the left, with L-arg phenylephrine dose response curve in the SHR group was not significantly Variety. Clearly shifted to the right in the WKY group. Conclusions (1) When α_1-adrenoceptor stimulated and induced vasoconstriction while causing vasoconstriction, it induced the increase of NO release from the endothelium; (2) NO release from the endothelium played a negative feedback role in vasoconstriction; and (3) Discharge of NO dysfunction is one of the causes of the increased reactivity of α 1 -adrenergic receptor agonists in vascular resistance.