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探讨ＮＯ系统和血管α１－肾上腺素受体α１－ＡＲ）及三磷酸肌醇受体（ＩＰ３Ｒ）系统在高血压发病中的相互作用。方法在常规饲食中加入Ｌ－ＮＡＭＥ喂饲大鼠１或４周制备大鼠高血压模型；应用放射性配基结合实验观察α１－ＡＲ及ＩＰ３Ｒ的变化。结果应用Ｌ－ＮＡＭＥ处理一周，大鼠动脉血压升高３０（２ｍｍＨｇ（Ｐ＜０．０５），血浆ＮＯｘ含量则下降２５％（Ｐ＜０．０５）。主动脉肌膜α１－ＡＲ及肌浆网ＩＰ３Ｒ密度分别增加１２％和４０％。Ｌ－ＮＡＭＥ处理４周，大鼠血压升高７５±８ｍｍＨｇ（Ｐ＜０．０１），血浆ＮＯｘ含量下降５０％（Ｐ＜０．０１），主动脉肌膜α１－ＡＲ及肌浆网ＩＰ３Ｒ密度分别较对照组高７３％和１３７％（Ｐ＜０．０１），此时尾动脉肌膜ＡＲ及肌浆网ＩＰ３Ｒ密度亦较对照组增加５５％和５６％（Ｐ＜０．０１）。结论提示长期抑制ＮＯＳ引起大鼠持续性高血压的同时，可致大鼠血管α１－ＡＲ及ＩＰ３Ｒ明显上调。
To investigate the interaction between NO system and vascular α1-adrenergic receptor α1-AR and IP3R system in the pathogenesis of hypertension. Methods The rat model of hypertension was established by feeding L-NAME to rats for 1 or 4 weeks. The changes of α1-AR and IP3R were observed by radioligand binding assay. Results After treated with L-NAME for one week, the arterial blood pressure increased by 30 mmHg (P <0.05), and the plasma NOx decreased by 25% (P <0.05) .A1-AR and sarcoplasmic sarcoplasmic reactivity The density of IP3R increased by 12% and 40%, respectively. L-NAME treatment for 4 weeks resulted in a 75 ± 8 mmHg increase in blood pressure (P <0.01) and a 50% decrease in plasma NO (P <0.01) The density of α1-AR and sarcoplasmic reticulum IP3R were 73% and 137% higher than that of the control group respectively (P <0.01). At this time, the density of IP3R in sarcolemmal sarcolemma and sarcoplasmic reticulum increased by 55% 56% (P <0.01) .Conclusions The results suggest that long-term inhibition of NOS-induced persistent hypertension in rats, can cause vascular α1-AR and IP3R significantly increased.