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)%(P0.05),该增殖作用由NPY Y
1
受体亚型介导。多巴胺D
1
类受体激动剂Fenoldopam对VSMCs无增殖影响,但Fenoldopam可抑制NPY Y
1
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D
1
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。
Abstract
Objective To determine the effect of D
1
-like dopamine receptor on neuropeptide Y (NPY)-mediated proliferation in primary cultured vascular smooth muscle cells (VSMCs) derived from thoracic aorta of Sprague-Dawley(SD) rats. Methods After VSMCs were isolated from SD rat thoracic aorta and identified by morphology and immunocytocchemistry
the cells at passage 4 to 8 were treated by 10
-8
t
o 10
-11
mol/L NPY in presence or absence of D
1
-like receptor agonist fenoldopam (10
-8
mol/L)
blocker BIBP3226(10
-6
mol/L)
or antagonist SCH23390 (10
-8
mol/L)to observe NPY-mediated proliferation in VSMCs. The proliferation of VSMCs was investigated by [
3
H
]
-TdR incorporation and MTT assay. Results NPY resulted in an increased proliferation of VSMCs in a concentration-dependent manner
with a maximal proliferative amplitude of (77±9)% (P0.05). D
1
-like receptor agonist
fenoldopam
completely blocked the NPY Y
1
-mediated proliferation in VSMCs
although the agonist had no effect on the proliferation of VSMCs by itself
which might be through protein kinase A pathway. Conclusion Activation of D
1
-like receptor inhibits NPY Y
1
-mediated proliferation in VSMCs,which might be involved in the pathogenesis of cardiovascular diseases.