一氧化氮在澳毒蛛（Androctonus australis）和犹太金蝎（Buthotus judaicus）蝎毒诱导的兔海绵体舒张中的作用。

The role of nitric oxide on the relaxations of rabbit corpus cavernosum induced by Androctonus australis and Buthotus judaicus scorpion venoms.

作者信息

Teixeira C E, Teixeira S A, Antunes E, De Nucci G

机构信息

Department of Pharmacology, Faculty of Medical Sciences, UNICAMP, P. O. Box 6111, 13081-970, (SP), Campinas, Brazil.

出版信息

Toxicon. 2001 May;39(5):633-9. doi: 10.1016/s0041-0101(00)00187-2.

DOI:10.1016/s0041-0101(00)00187-2

PMID:11072041

Abstract

In this study, we have investigated the relaxing effects of both Androctonus australis venom (AAV) and Buthotus judaicus venom (BJV) on the rabbit corpus cavernosum (RbCC) smooth muscle strips. The RbCC strips were mounted in a cascade system and superfused with warmed and gassed Krebs solution. The nitric oxide (NO) synthesis inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME, 10microM), but not D-NAME (10microM), significantly inhibited the RbCC relaxations induced by acetylcholine (ACh, 0.6nmol), AAV (30microg) and BJV (30microg). Subsequent infusion of L-arginine (300microM), but not of D-arginine (300microM), partially restored the relaxations evoked by these agents. The brain NO synthase inhibitor 7-nitroindazole (7-NI, 10microM) also inhibited the relaxant responses elicited by the scorpion venoms. The guanylyl cyclase inhibitors methylene blue (MB, 30microM) and 1H-[1,2,4] oxadiazolo [4,3,-alquinoxalin-1-one] (ODQ, 10microM) virtually abolished the relaxations induced by either AAV or BJV. The infusion of muscarinic receptor antagonists such as scopolamine and atropine (1microM, each) completely abolished the ACh-induced relaxations but had no effect on those evoked by the scorpion venoms. The Na(+) channel blocker tetrodotoxin (1microM) prevented the relaxations evoked by both AAV and BJV. Thus, NO released from nitrergic nerve fibres mediates the relaxations elicited by AAV and BJV in the rabbit cavernosal tissue.

摘要

在本研究中，我们研究了澳毒蛛毒液（AAV）和犹大杀牛蝎毒液（BJV）对兔海绵体（RbCC）平滑肌条的舒张作用。将RbCC条安装在级联系统中，并用温热且通有气体的 Krebs 溶液进行灌流。一氧化氮（NO）合成抑制剂N（ω）-硝基-L-精氨酸甲酯（L-NAME，10μM），而非D-NAME（10μM），能显著抑制由乙酰胆碱（ACh，0.6nmol）、AAV（30μg）和BJV（30μg）诱导的RbCC舒张。随后输注L-精氨酸（300μM），而非D-精氨酸（300μM），可部分恢复这些药物引起的舒张。脑型NO合酶抑制剂7-硝基吲唑（7-NI，10μM）也能抑制蝎毒引起的舒张反应。鸟苷酸环化酶抑制剂亚甲蓝（MB，30μM）和1H-[1,2,4]恶二唑并[4,3,-a]喹喔啉-1-酮（ODQ，10μM）几乎完全消除了由AAV或BJV诱导的舒张。输注毒蕈碱受体拮抗剂如东莨菪碱和阿托品（各1μM）可完全消除ACh诱导的舒张，但对蝎毒引起的舒张无影响。钠（Na⁺）通道阻滞剂河豚毒素（1μM）可阻止AAV和BJV引起的舒张。因此，由含氮能神经纤维释放的NO介导了AAV和BJV在兔海绵体组织中引起的舒张。