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环磷酸腺苷磷酸二酯酶抑制剂对豚鼠气管的舒张作用及其被硝普钠增强的作用

Relaxation of guinea-pig trachea by cyclic AMP phosphodiesterase inhibitors and their enhancement by sodium nitroprusside.

作者信息

Turner N C, Lamb J, Worby A, Murray K J

机构信息

SmithKline Beecham Pharmaceuticals, The Frythe, Welwyn, Herts.

出版信息

Br J Pharmacol. 1994 Apr;111(4):1047-52. doi: 10.1111/j.1476-5381.1994.tb14850.x.

Abstract
  1. The effects of agents that elevate either cyclic AMP (the phosphodiesterase (PDE) III inhibitor siguazodan, salbutamol) or cyclic GMP (sodium nitroprusside (SNP)) on the relaxant activity of the PDE IV inhibitor, rolipram, were investigated in carbachol (0.1 microM) precontracted guinea-pig tracheal sheets. 2. Rolipram, siguazodan and SNP caused concentration-related reductions in tone of tissues precontracted with 0.1 microM carbachol (EC50 values 12.5; 2.73 and 0.35 microM respectively). Whilst the concentration-response relationship for the PDE III inhibitor, siguazodan, was monophasic that of the PDE IV inhibitor, rolipram, was biphasic. 3. The relaxant activity of rolipram was markedly enhanced in the presence of 10 microM siguazodan (EC50 < 0.01 microM), 0.1 microM salbutamol (EC50 0.03 microM) and 0.3 microM SNP (EC50 0.03 microM). In contrast, the relaxant activity of siguazodan was unaffected by SNP and only modestly enhanced by rolipram (10 microM) and salbutamol (0.1 microM). 4. The relaxant activity of SNP was enhanced by the PDE V inhibitor SK&F 96231 (30 microM: EC50 0.06 microM) and rolipram (30 microM, EC50 0.08 microM) but was unaffected by 30 microM siguazodan. 5. At concentrations up to 10 microM, neither siguazodan nor rolipram elevated tracheal cyclic AMP levels. However, the combination of 10 microM rolipram and siguazodan caused a two fold increase in the cyclic AMP content (from 2.19 to 4.36 pmol cyclic AMP mg-1 protein). SNP (0.1-10 microM) failed to produce a significant increase in tracheal cyclic AMP levels. At 0.1 microM the effect of SNP on tracheal cyclic AMP levels was significantly (P < 0.05) increased in the presence of rolipram but not siguadozan. 6. The results indicate that the relaxant effects of rolipram are markedly enhanced by agents that inhibit PDE III activity or elevate cyclic GMP. They support the hypothesis that SNP potentiates the effects of rolipram via the inhibitory action of cyclic GMP on hydrolysis of cyclic AMP by PDE III. The findings also suggest that whilst PDE III may be more significant in regulating basal smooth muscle tone in the absence of any exogenous stimulus to cyclic AMP accumulation, PDE IV activity may be more tightly coupled to the pool of adenylyl cyclase stimulated by beta2-adrenoceptor agonists.
摘要
  1. 在豚鼠气管片预先用卡巴胆碱(0.1微摩尔)收缩的情况下,研究了升高环磷酸腺苷(磷酸二酯酶(PDE)III抑制剂西呱唑旦、沙丁胺醇)或环磷酸鸟苷(硝普钠(SNP))的药物对PDE IV抑制剂咯利普兰舒张活性的影响。2. 咯利普兰、西呱唑旦和SNP使预先用0.1微摩尔卡巴胆碱收缩的组织张力呈浓度依赖性降低(EC50值分别为12.5、2.73和0.35微摩尔)。PDE III抑制剂西呱唑旦的浓度-反应关系是单相的,而PDE IV抑制剂咯利普兰的浓度-反应关系是双相的。3. 在存在10微摩尔西呱唑旦(EC50<0.01微摩尔)、0.1微摩尔沙丁胺醇(EC50 0.03微摩尔)和0.3微摩尔SNP(EC50 0.03微摩尔)时,咯利普兰的舒张活性显著增强。相比之下,西呱唑旦的舒张活性不受SNP影响,仅被咯利普兰(10微摩尔)和沙丁胺醇(0.1微摩尔)适度增强。4. PDE V抑制剂SK&F 96231(30微摩尔:EC50 0.06微摩尔)和咯利普兰(30微摩尔,EC50 0.08微摩尔)增强了SNP的舒张活性,但30微摩尔西呱唑旦对其无影响。5. 浓度高达10微摩尔时,西呱唑旦和咯利普兰均未升高气管环磷酸腺苷水平。然而,10微摩尔咯利普兰和西呱唑旦的组合使环磷酸腺苷含量增加了两倍(从2.19皮摩尔环磷酸腺苷毫克-1蛋白增加到4.36皮摩尔)。SNP(0.1 - 10微摩尔)未能使气管环磷酸腺苷水平显著升高。在0.1微摩尔时,在存在咯利普兰而非西呱唑旦的情况下,SNP对气管环磷酸腺苷水平的影响显著(P<0.05)增加。6. 结果表明,抑制PDE III活性或升高环磷酸鸟苷的药物可显著增强咯利普兰的舒张作用。它们支持这样的假说,即SNP通过环磷酸鸟苷对PDE III水解环磷酸腺苷的抑制作用来增强咯利普兰的作用。研究结果还表明,虽然在没有任何外源性刺激使环磷酸腺苷积累的情况下,PDE III在调节基础平滑肌张力方面可能更重要,但PDE IV活性可能与β2-肾上腺素能激动剂刺激的腺苷酸环化酶池更紧密相关。

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