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一氧化氮和鸟苷 3',5'-环磷酸在介导豚鼠肺动脉非肾上腺素能、非胆碱能舒张中的作用。

Role of nitric oxide and guanosine 3',5'-cyclic monophosphate in mediating nonadrenergic, noncholinergic relaxation in guinea-pig pulmonary arteries.

作者信息

Liu S F, Crawley D E, Rohde J A, Evans T W, Barnes P J

机构信息

Department of Thoracic Medicine, National Heart and Lung Institute, London.

出版信息

Br J Pharmacol. 1992 Nov;107(3):861-6. doi: 10.1111/j.1476-5381.1992.tb14538.x.

Abstract
  1. Nonadrenergic, noncholinergic (NANC) nerves mediate vasodilatation in guinea-pig pulmonary artery (PA) by both endothelium-dependent and endothelium-independent mechanisms. The transmitter(s) involved in the endothelium-independent pathway have not yet been identified. We have therefore investigated the possibility that nitric oxide (NO) and guanosine 3',5'-cyclic monophosphate (cyclic GMP) may mediate this neural vasodilator response in guinea-pig branch PA rings denuded of endothelium. 2. Electric field stimulation (EFS, 50 V, 0.2 ms) induced a frequency-dependent (1-24 Hz), tetrodotoxin-sensitive relaxation of the U44069-precontracted PA rings in the presence of adrenergic and cholinergic blockade. 3. The NO synthase inhibitors NG-monomethyl L-arginine (L-NMMA, 100 microM) and NG-nitro L-arginine methyl ester (L-NAME, 30 microM), and the guanylyl cyclase inhibitor methylene blue (5 microM) inhibited the EFS (16 Hz)-induced relaxation by 53 +/- 5, 74 +/- 9 and 82 +/- 9% respectively (n = 5-7, P < 0.01, compared with control rings). 4. Excess concentrations of L-, but not D-arginine (300 microM) completely reversed the inhibitory effect of L-NMMA. 5. The EFS-elicited relaxation (4 Hz) was potentiated by 1 microM zaprinast, a type V phosphodiesterase inhibitor which inhibits guanosine 3':5'-cyclic monophosphate (cyclic GMP) degradation, but was unaffected by 0.1 microM zardaverine, a type III/IV phosphodiesterase inhibitor which inhibits cyclic AMP degradation. 6. EFS (50 V, 0.2 ms, 16 Hz) induced a 3 fold increase in tissue cyclic GMP content, an action which was inhibited by L-NMMA (100 microM). 7. Pyrogallol (100microM), a superoxide anion generator, also inhibited the EFS-induced relaxation by 53 +/- 9%, and this effect was prevented by superoxide dismutase.8. Chemical sympathetic denervation with 6-hydroxydopamine had no effect on the relaxant response to EFS in the endothelium-denuded PA rings.9. In endothelium-denuded branch PA rings at resting tone, L-NMMA (100 microM) significantly augmented the adrenergic contractile response, an effect which was completely reversed by L-arginine,but not by D-arginine. In the same groups of vessel rings, L-NMMA had no significant effect on the matched contractile response to exogenous noradrenaline.10. These results suggest that NO may be released from intramural nerve endings other than adrenergic nerves (probably NANC nerves), and this leads to vasodilatation via activation of guanylyl cyclase.
摘要
  1. 非肾上腺素能、非胆碱能(NANC)神经通过内皮依赖性和非内皮依赖性机制介导豚鼠肺动脉(PA)血管舒张。参与非内皮依赖性途径的递质尚未确定。因此,我们研究了一氧化氮(NO)和鸟苷3',5'-环磷酸(环鸟苷酸)是否可能介导内皮剥脱的豚鼠分支PA环中的这种神经血管舒张反应。2. 在存在肾上腺素能和胆碱能阻断的情况下,电场刺激(EFS,50V,0.2ms)诱导U44069预收缩的PA环出现频率依赖性(1 - 24Hz)、对河豚毒素敏感的舒张。3. NO合酶抑制剂NG-单甲基-L-精氨酸(L-NMMA,100μM)和NG-硝基-L-精氨酸甲酯(L-NAME,30μM)以及鸟苷酸环化酶抑制剂亚甲蓝(5μM)分别抑制EFS(16Hz)诱导的舒张达53±5%、74±9%和82±9%(n = 5 - 7,与对照环相比,P < 0.01)。4. 过量的L-精氨酸(300μM)而非D-精氨酸完全逆转了L-NMMA的抑制作用。5. 1μM扎普司特(一种抑制鸟苷3':5'-环磷酸(环鸟苷酸)降解的V型磷酸二酯酶抑制剂)增强了EFS诱导的舒张(4Hz),但0.1μM扎达维林(一种抑制环磷酸腺苷降解的III/IV型磷酸二酯酶抑制剂)对其无影响。6. EFS(50V,0.2ms,16Hz)使组织环鸟苷酸含量增加3倍,但该作用被L-NMMA(100μM)抑制。7. 焦性没食子酸(100μM),一种超氧阴离子生成剂,也抑制EFS诱导的舒张达53±9%,且该作用被超氧化物歧化酶阻止。8. 用6-羟基多巴胺进行化学性交感神经去支配对内皮剥脱的PA环中EFS的舒张反应无影响。9. 在静息张力下的内皮剥脱分支PA环中,L-NMMA(100μM)显著增强肾上腺素能收缩反应,该作用被L-精氨酸完全逆转,但不被D-精氨酸逆转。在同一组血管环中,L-NMMA对外源性去甲肾上腺素的匹配收缩反应无显著影响。10. 这些结果表明,NO可能从肾上腺素能神经以外的壁内神经末梢(可能是NANC神经)释放,并通过激活鸟苷酸环化酶导致血管舒张。

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