人类血管平滑肌细胞表达本构一氧化氮合酶胰岛素迅速激活,从而增加3”:5 '环鸟苷一磷酸腺苷3”:5 '环一磷酸浓度。
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Trovati M, Massucco P, Mattiello L, Costamagna C, Aldieri E, F Cavalot, Anfossi G,邦仕嘉,Ghigo D
人类血管平滑肌细胞表达本构一氧化氮合酶胰岛素迅速激活,从而增加3”:5 '环鸟苷一磷酸腺苷3”:5 '环一磷酸浓度。
Diabetologia。1999年7月,42 (7):831 - 9。
- PubMed ID
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10440125 (在PubMed]
- 文摘
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目的/假说:胰岛素孵化的人类血管平滑肌细胞(hVSMC) 120分钟增加3”:5 '环鸟苷一磷酸腺苷(cGMP)和3”:5 '环一磷酸(营),这些影响被抑制一氧化氮合酶(NOS)。这些数据表明,胰岛素激活本构Ca2 +端依赖NOS(碳氮氧),在hVSMC没有描述。为了验证这个假设,我们评估hVSMC: i)的动力学insulin-induced两环核苷酸的增强;(二)一氧化氮(NO)的能力来增加环核苷酸;3)没有参与胰岛素两环核苷酸的短期影响;(四)胰岛素的能力增加没有生产在几分钟内;v)的碳氮氧活动;(六)对碳氮氧mRNA的表达。方法:在hVSMC孵化与胰岛素,没有捐赠者和Ca2 +离子载体ionomycin,我们测量营地和cGMP (RIA);与胰岛素和hVSMC孵化ionomycin我们测量不,评为L - (3 h)瓜氨酸生产从L -精氨酸(3 h); by northern blot hybridization, we measured the expression of cNOS mRNA. RESULTS: i) By incubating hVSMC with 2 nmol/l insulin for 0-240 min, we observed an increase of both cGMP and cAMP (ANOVA: p = 0.0001). Cyclic GMP rose from 0.74 +/- 0.01 to 2.62 +/- 0.10 pmol/10(6) cells at 30 min (p = 0.0001); cAMP rose from 0.9 +/- 0.09 to 11.65 +/- 0.74 pmol/10(6) cells at 15 min (p=0.0001). ii) Sodium nitroprusside (100 mol/l) and glyceryltrinitrate (100 micromol/l) increased both cGMP and cAMP (p = 0.0001). iii) The effects of insulin on cyclic nucleotides were blocked by NOS inhibition. iv) An increase of NO was observed by incubating hVSMC for 5 min with 2 nmol/l insulin (p = 0.0001). v) Ionomycin (1 micromol/l) enhanced NO production (p = 0.0001) and increased both cyclic nucleotides (p = 0.0001). vi) hVSMC expressed mRNA of cNOS. CONCLUSION/INTERPRETATION: Human VSMC express cNOS, which is rapidly activated by insulin with a consequent increase of both cGMP and cAMP, suggesting that insulin-induced vasodilation in vivo is not entirely endothelium-mediated.