Morimoto S, Nabata T, Fukuo K, Yasuda O, Inoue T, Momose N, Koh E, Kitano S, Tamatani M, Ogihara T
Department of Geriatric Medicine, Osaka University Medical School, Japan.
Blood Press Suppl. 1992;3:27-9.
The effects of manidipine hydrochloride, a calcium channel blocker, on the proliferation and the synthesis of glycosaminoglycans (GAG) in cultured rat aortic vascular smooth muscle cells (VSMC) were studied. Mandipine hydrochloride suppressed the DNA synthesis of VSMC dose dependently at concentrations of more than 10(-8) M. Mandipine hydrochloride 10(-6) M suppressed proliferation of VSMC to 50% of the control value. Manidipine hydrochloride stimulated the synthesis of GAG at concentrations above 10(-11) M. Manidipine hydrochloride 10(-8) M stimulated synthesis of GAG to 450% of control. Our findings suggest that because mandipine hydrochloride suppresses proliferation and stimulates GAG synthesis of VSMC, it may be an anti-arteriosclerotic agent.
研究了钙通道阻滞剂盐酸马尼地平对培养的大鼠主动脉血管平滑肌细胞(VSMC)增殖和糖胺聚糖(GAG)合成的影响。盐酸马尼地平在浓度高于10^(-8) M时剂量依赖性地抑制VSMC的DNA合成。10^(-6) M的盐酸马尼地平将VSMC的增殖抑制至对照值的50%。盐酸马尼地平在浓度高于10^(-11) M时刺激GAG的合成。10^(-8) M的盐酸马尼地平将GAG的合成刺激至对照的450%。我们的研究结果表明,由于盐酸马尼地平抑制VSMC的增殖并刺激其GAG合成,它可能是一种抗动脉粥样硬化药物。