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第4～8代离体培养的SD大鼠胸主动脉平滑肌细胞(VSMCs),用人白细胞介素-1β(hIL-1β,200U/ml)诱导NO生成,并研究其对血管紧张素Ⅱ(ANGⅡ,100U/ml)介导VSMC[Ca~(2+)]i升高反应的影响。结果:(1) VSMC源性亚硝酸盐(一种NO代谢产物)基础生成量为2.24-±0.52 nmol/10~6 cells·24h~(-1)(n=12),hlL-1β诱导后生成量为44.5±4.7nmol/10~6 cells·24h~(-1)(n=12,P<0.001);(2) 一氧化氮合成酶抑制剂L-NAME(10～150μmol/L)剂量依赖性抑制hIL-1β诱导的VSMC源性NO生成;(3) 基础及hIL-1β诱导的VSMC源性NO生成,对ANGⅡ介导的VSMC[Ca~(2+)]i升高均具有明显抑制作用。提示VSMC源性NO对自身细胞内钙升高具有自分泌抑制作用。
The generation of NO was induced by human interleukin-1β (200U / ml) on the fourth and eighth generation of SD rat thoracic aortic smooth muscle cells (VSMCs) in vitro and the effects on angiotensin Ⅱ , 100U / ml) mediated VSMC [Ca ~ (2 +)] i increased response. RESULTS: The basal production of VSMC-derived nitrite (a NO metabolite) was 2.24- ± 0.52 nmol / 10-6 cells · 24h -1 (n = 12). After induction of hlL- (N = 12, P <0.001). (2) The dose of L-NAME (10-150 μmol / L), a nitric oxide synthase inhibitor, was 44.5 ± 4.7 nmol / Dependent inhibition of hIL-1β-induced VSMC-derived NO production; (3) basal and hIL-1βinduced VSMC-derived NO production, ANG Ⅱ -mediated VSMC [Ca ~ (2 +)] i increased significantly Inhibition. These results suggest that VSMC-derived NO has an autocrine inhibitory effect on intracellular calcium elevation.