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异丙肾上腺素和一氧化氮合酶抑制剂对大鼠唾液腺导管的不同作用。

Different role of isoproterenol and NOS inhibitors on salivary ducts of rats.

作者信息

Issy A C, da Silva C A, Guimarães F S, Del Bel E A

机构信息

Department of Pharmacology, University of São Paulo, Av. Bandeirantes 13400, 14049-900 Ribeirão Preto, SP, Brazil.

出版信息

Micron. 2009 Apr;40(3):343-9. doi: 10.1016/j.micron.2008.10.007. Epub 2008 Nov 1.

DOI:10.1016/j.micron.2008.10.007
PMID:19167231
Abstract

OBJECTIVES

Nitric oxide (NO) is a diffusible intracellular messenger that is present in saliva. Chronic treatment with isoproterenol, a beta receptor agonist, stimulates the release of NO from acinar cells and induces salivary gland hypertrophy. The aim of this study was to investigate the effect of NO synthesis inhibitors and isoproterenol on rat salivary glands. We analyzed salivary gland weight and the number of ducts per unit area (0.5mm(2)) by NADPH-diaphorase histochemistry (to identify the presence of the enzyme NO synthase-NOS) and haematoxylin-and-eosin (HE).

METHODS

For 8 days male Wistar rats received daily single intraperitoneal injections of saline or a NOS inhibitor (40mg/kg N(omega)-nitro-L-arginine L-NOARG or N(omega)-nitro-l-arginine methyl ester L-NAME). This was followed, 30min later, by subcutaneous injection of isoproterenol (2 or 5mg/kg) or saline.

RESULTS

Isoproterenol increased parotid and submandibular gland weights. Isoproterenol (2mg/kg) induced a decrease of ducts per unit area inversely correlated to the weight of the parotid gland. This effect was augmented by L-NAME. In the submandibular gland L-NAME attenuated isoproterenol (2mg/kg) weight increase. In the submandibular gland isoproterenol and NOS inhibitors induced an increase in ducts per unit area (HE and NADPH-diaphorase). No effect was observed in the sublingual gland.

CONCLUSION

To our knowledge this is the first description of isoproterenol and NOS inhibitors increasing duct density in the submandibular gland. Our results corroborate the hypothesis that NO plays different roles in parotid and submandibular glands.

摘要

目的

一氧化氮(NO)是一种存在于唾液中的可扩散细胞内信使。用β受体激动剂异丙肾上腺素进行长期治疗,可刺激腺泡细胞释放NO并诱导唾液腺肥大。本研究的目的是探讨NO合成抑制剂和异丙肾上腺素对大鼠唾液腺的影响。我们通过NADPH-黄递酶组织化学法(以鉴定一氧化氮合酶-NOS的存在)和苏木精-伊红(HE)染色分析了唾液腺重量和单位面积(0.5mm²)的导管数量。

方法

雄性Wistar大鼠连续8天每日单次腹腔注射生理盐水或一氧化氮合酶抑制剂(40mg/kg Nω-硝基-L-精氨酸-L-NOARG或Nω-硝基-L-精氨酸甲酯-L-NAME)。30分钟后,皮下注射异丙肾上腺素(2或5mg/kg)或生理盐水。

结果

异丙肾上腺素增加了腮腺和颌下腺的重量。异丙肾上腺素(2mg/kg)导致单位面积导管数量减少,这与腮腺重量呈负相关。L-NAME增强了这种作用。在颌下腺中,L-NAME减弱了异丙肾上腺素(2mg/kg)引起的重量增加。在颌下腺中,异丙肾上腺素和一氧化氮合酶抑制剂导致单位面积导管数量增加(HE和NADPH-黄递酶染色)。舌下腺未观察到影响。

结论

据我们所知,这是首次描述异丙肾上腺素和一氧化氮合酶抑制剂增加颌下腺导管密度。我们的结果证实了NO在腮腺和颌下腺中发挥不同作用的假说。

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