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目的探讨多巴胺D1类受体对神经肽Y(neuropeptide Y,NPY)受体介导的Sprague-Dawley(SD)大鼠原代血管平滑肌细胞(vascular smooth muscle cells,VSMCs)增殖的影响。方法以NPY(10-8～10-11mol/L)刺激SD大鼠胸主动脉培养的VSMCs,观察在D1类多巴胺受体激动剂Fenoldopam(10-8mol/L)存在的情况下,神经肽Y促VSMCs增殖作用的变化。细胞增殖的检测采用[3H]胸腺嘧啶核苷([3H]-TdR)掺入率的变化表示及MTT方法。结果 NPY呈浓度依赖性促进SD大鼠VSMCs的异常增殖,最高增殖幅度达(77±9)%(P<0.05),该增殖作用由NPY Y1受体亚型介导。多巴胺D1类受体激动剂Fenoldopam对VSMCs无增殖影响,但Fenoldopam可抑制NPY Y1亚型受体介导VSMCs的增殖作用,该作用通过PKA途径发挥作用。结论多巴胺D1类受体激活抑制NPY受体介导的促VSMCs增殖作用,可能参与心血管疾病的发生、发展过程。
Objective To investigate the effects of dopamine D1 receptors on proliferation of primary smooth muscle cells (VSMCs) of Sprague-Dawley rats induced by neuropeptide Y (NPY) receptor. Methods VSMCs cultured in the thoracic aorta of SD rats were stimulated with NPY (10-8 ~ 10-11mol / L). In the presence of Fenoldopam (10-8mol / L), a D1 dopamine receptor agonist, neuropeptide Y Proliferation of VSMCs. Cell proliferation was measured using the change in incorporation of [3H] thymidine ([3H] -TdR) and the MTT assay. Results NPY promoted the proliferation of SD rat VSMCs in a concentration-dependent manner with the highest proliferation rate of 77 ± 9% (P <0.05). The proliferative effect was mediated by the NPY Y1 receptor subtype. Fenoldopam, a dopamine D1 receptor agonist, has no effect on proliferation of VSMCs, but Fenoldopam can inhibit the proliferation of VSMCs mediated by the NPY Y1 subtype receptor, which acts via the PKA pathway. Conclusion Activation of dopamine D1 receptors can inhibit NPY receptor-mediated proliferation of VSMCs, which may be involved in the pathogenesis and progression of cardiovascular diseases.