摘要
目的观察D1类多巴胺受体对肾上腺素α受体介导的血管平滑肌（VSM）细胞增殖的影响。方法以去甲肾上腺素（NE）10^-6～10^-9mol／L刺激Sprague-Dawley（SD）大鼠主动脉分离的VSM细胞，观察在D。类多巴胺受体激动剂（Fenoldopam）10^-5～10^-8mol／L存在的情况下，NE促细胞增殖作用的变化，细胞增殖用。H-TdR掺人量表示。结果NE呈浓度依赖性的促进SD大鼠VSM细胞的增殖，该作用由肾上腺素α受体介导，酚妥拉明存在的情况下可消除NE的促增殖作用。Fenoldopam本身对VSM细胞增殖无影响，但Fenoldopam可通过D1类多巴胺受体减弱NE（10^-6mol／L）介导的VSM细胞增殖；该实验结果得到了人VSM细胞实验结果的印证。结论D-类多巴胺受体对NE介导的促VSM细胞增殖具有抑制作用，该作用可能在高血压的发生、发展中发挥一定的作用。
Objective To determine the effect of D1-like receptor on α-adrenergic receptor-mediated proliferation of vascular smooth muscle （VSM） cells derived from aorta in SD rats. Methods The primary cultured VSM cells were treated by norepinephrine （NE）10^-6- 10^-9 mol/L with or without the presence of D1-like dopamine receptor agonist, fenoldopam 10^-6 -10^-9 mol/L. The proliferation of VSM cells was determined by ^3 HTdR incorporation. Results NE dose-dependently increased proliferation of primary cultured VSM cells from aorta of Sprague-Dawley rats. α-Adrenergic receptor blocker, phentolamine, blocked the stimulatory effect of NE on VSM cell proliferation with little effect by itself, D1-like dopamine receptor agonist, fenoldopam, reduced the stimulatory effect of NE on VSM cell proliferation with little effect by itselt. The above-mentioned effects were confirmed in primary cultured VSM cells from human mesenteric arteries. Conclusion Activation of D1 like dopamine receptor reduces the stimulatory effect of NE on VSM cell proliferation, which may take part into the pathogenesis of essential hypertension.
出处
《中华高血压杂志》
CAS
CSCD
北大核心
2007年第1期57-60,共4页
Chinese Journal of Hypertension
基金
国家自然基金资助项目(30470728
30672199)
