Modin A, Weitzberg E, Lundberg J M
Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Eur J Pharmacol. 1994 Aug 11;261(1-2):185-97. doi: 10.1016/0014-2999(94)90318-2.
The possible involvement of nitric oxide (NO) in the vasodilator response to parasympathetic nerve stimulation in the pig submandibular gland in vivo was studied using the NO synthase inhibitor, NG-nitro-L-arginine. The atropine-resistant vasodilation elicited by parasympathetic stimulation (10 Hz, 30 s) and the response elicited by i.v. injection of vasoactive intestinal polypeptide (VIP) were markedly reduced by NG-nitro-L-arginine. Furthermore, peptide release from the gland elicited by nerve stimulation was attenuated after NG-nitro-L-arginine administration. Addition of the NO donor, nitroprusside, reversed the NG-nitro-L-arginine evoked attenuation of the response to nerve stimulation and VIP. Also the cholinergic parasympathetic component and the vascular effect of acetylcholine were reduced by NG-nitro-L-arginine. Furthermore, the NG-nitro-L-arginine-induced attenuation of the vascular responses was partially prevented by milrinone, an inhibitor of the cyclic GMP-regulated phosphodiesterase III. The present results suggest that NO may be crucial for parasympathetic vasodilatation by regulating peptide release and second messenger systems for VIP and acetylcholine.
利用一氧化氮合酶抑制剂NG-硝基-L-精氨酸，研究了一氧化氮（NO）在猪下颌下腺体内对副交感神经刺激的血管舒张反应中可能的作用。副交感神经刺激（10Hz，30s）引起的阿托品抵抗性血管舒张以及静脉注射血管活性肠肽（VIP）引起的反应，均被NG-硝基-L-精氨酸显著降低。此外，给予NG-硝基-L-精氨酸后，神经刺激引起的腺体肽释放减弱。添加NO供体硝普钠可逆转NG-硝基-L-精氨酸引起的对神经刺激和VIP反应的减弱。NG-硝基-L-精氨酸还降低了胆碱能副交感成分和乙酰胆碱的血管效应。此外，环磷酸鸟苷调节的磷酸二酯酶III抑制剂米力农可部分阻止NG-硝基-L-精氨酸诱导的血管反应减弱。目前的结果表明，NO可能通过调节肽释放以及VIP和乙酰胆碱的第二信使系统，对副交感神经血管舒张至关重要。
