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作 者:符民桂[1] 杨军[1] 庞永政 唐朝枢[1] 刘乃奎[1]
出 处:《高血压杂志》1998年第4期291-295,共5页Chinese Journal of Hypertension
基 金:国家自然基金
摘 要: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。Aim\ This study was designed to investigate the relationship of NO system and α 1 adrenoceptor and inositol trisphosphate receptor systems in hypertension.\ Methods\ The model of NOS inhibition induced rat hypertension was prepared by treating with L NAME for 1 or 4 weeks, and the binding of α 1 adrenoceptor and inositol trisphosphate receptor was determined by radioactive ligand binding assay.\ Results\ It was found that in the rats treated with L NAME for 1 week, the blood pressure was significantly increased by 30±2 mmHg( P <0.05) than that in control group, and the plasma Nox levels was decreased by 25%( P <0.05). Meanwhile, the density of α 1 adrenoceptor and inositol trisphosphate receptor in the aorta were significantly increased by 12% and 40% respectivly; no changes was found in the caudal artery. In the rats treated with L NAME for 4 weeks,the blood pressure was increased by 75±8 mmHg( P <0.01) than that in control group, and the plasma NOx levels was decreased by 50%( P <0.01). Meanwhile, the density of α 1 adrenoceptor and inositol trisphosphate receptor increase further more in the aorta, and the alteration was found in the caudal artery as well.\ Conclusion\ NOS inhibition upregulates the α 1 adrenoceptor and inositol trisphosphate receptor in rat arteries.
分 类 号:R544.1[医药卫生—心血管疾病]
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