Bottaro D, Shepro D, Peterson S, Hechtman H B
Am J Physiol. 1985 Mar;248(3 Pt 1):C252-7. doi: 10.1152/ajpcell.1985.248.3.C252.
The effects of serotonin (5-HT), histamine (H), and norepinephrine (NE) on bovine aortic endothelial cell (BAE) and vascular smooth muscle cell (VSM) movement were quantitated using a phagokinetic tracking assay. BAE movement was significantly reduced by 5-HT (31%), H (48%), and NE (62%) at concentrations ranging from 10(-10) to 10(-4) M (P less than 0.01). VSM motility was significantly enhanced by 5-HT (17%) and H (25%) at concentrations of 10(-8) and 10(-4)M, respectively (P less than 0.01). NE (10(-4)M) reduced VSM motility by 63% (P less than 0.01). Ketanserin (1 microM) reduced the 5-HT-associated inhibition of BAE movement by 75% (P less than 0.01). Diphenhydramine (1 microM) reduced the H-associated inhibition of BAE movement by 66% (P less than 0.01). Propranolol (1 microM) reduced NE-associated inhibition of BAE movement by 50% (P less than 0.01) and 5-HT-associated inhibition by 45% (P less than 0.05), but phenoxybenzamine had no significant effect. The results suggest 1) BAE and VSM are affected qualitatively in opposite ways by 5-HT and H; 2) the H-associated inhibition of BAE movement appears to be at least partially mediated by H1 receptors; 3) the 5-HT-associated inhibition of BAE movement may be mediated directly by a 5-HT binding component but indirectly by beta-adrenergic receptors; and 4) the NE-associated inhibition of BAE movement appears to be mediated by beta-adrenergic receptors.
采用吞噬动力学追踪试验对血清素(5-羟色胺,5-HT)、组胺(H)和去甲肾上腺素(NE)对牛主动脉内皮细胞(BAE)及血管平滑肌细胞(VSM)运动的影响进行了定量分析。在浓度范围为10⁻¹⁰至10⁻⁴M时,5-HT(31%)、H(48%)和NE(62%)可使BAE运动显著降低(P<0.01)。在浓度分别为10⁻⁸和10⁻⁴M时,5-HT(17%)和H(25%)可使VSM运动显著增强(P<0.01)。NE(10⁻⁴M)可使VSM运动降低63%(P<0.01)。酮色林(1微摩尔)可使5-HT相关的BAE运动抑制降低75%(P<0.01)。苯海拉明(1微摩尔)可使H相关的BAE运动抑制降低66%(P<0.01)。普萘洛尔(1微摩尔)可使NE相关的BAE运动抑制降低50%(P<0.01),使5-HT相关的抑制降低45%(P<0.05),但酚苄明无显著作用。结果表明:1)5-HT和H对BAE和VSM的影响在性质上相反;2)H相关的BAE运动抑制似乎至少部分由H1受体介导;3)5-HT相关的BAE运动抑制可能直接由5-HT结合成分介导,但间接由β-肾上腺素能受体介导;4)NE相关的BAE运动抑制似乎由β-肾上腺素能受体介导。