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目的观察D3多巴胺受体对肾上腺素α受体介导的血管平滑肌细胞(VSMC)增殖的影响。方法用去甲肾上腺素(NE)刺激SD大鼠的VSMC,观察在D3受体激动剂(PD128907)存在的情况下,NE促增殖作用的变化,其中细胞增殖用3H-TdR掺入量表示。结果NE通过肾上腺素α受体促进SD大鼠VSMC增殖,该作用呈现浓度依赖性关系。PD128907低浓度(10-8、10-7mol/L)对VSMC增殖无影响,但高浓度(10-6、10-5mol/L)却促进VSMC的增殖[PD128907 10-6mol/L=(4982±529)计数/min、PD128907 10-5mol/L=(5782±483)计数/min与对照=(3798±438)计数/min相比,P<0.05],此作用可被α受体阻断剂酚妥拉明阻断。低浓度的PD128907(10-7mol/L)可通过D3受体减弱NE 10-6mol/L引起的VSMC增殖[NE 10-6mol/L=(6315±245)计数/min与NE 10-6mol/L+PD128907 10-7mol/L=(4898±286)计数/min相比,P<0.05。结论D3受体对NE所致的VSMC增殖具有抑制作用,该作用可能在高血压的发生、发展中发挥作用。
Objective To observe the effect of D3 dopamine receptor on the proliferation of adrenergic receptor-mediated vascular smooth muscle cells (VSMCs). Methods VSMCs of SD rats were stimulated with norepinephrine (NE). The proliferative effect of NE was observed in the presence of D3 receptor agonist (PD128907), and the cell proliferation was expressed in 3H-TdR incorporation. Results NE promoted the proliferation of SD rat VSMC via adrenaline α receptor in a dose-dependent manner. Low concentration of PD128907 (10-8,10-7mol / L) had no effect on VSMC proliferation, but high concentration (10-6,10-5mol / L) promoted VSMC proliferation [PD128907 10-6mol / L = (4982 ± 529) / min, PD128907 10-5mol / L = (5782 ± 483) counts / min vs control = (3798 ± 438 counts / min, P <0.05] Phentolamine blocks. Low concentrations of PD128907 (10-7 mol / L) attenuated NE 10-6 mol / L VSMC proliferation via the D3 receptor [NE 10-6 mol / L = (6315 ± 245) counts / min vs. NE 10-6 mol / L + PD128907 10-7mol / L = (4898 ± 286) counts / min, P <0.05. Conclusion D3 receptor can inhibit the proliferation of NE induced VSMC, which may play a role in the occurrence and development of hypertension.