Busch Lucila, Sterin-Borda Leonor, Borda Enri
Pharmacology Unit, School of Dentistry, University of Buenos Aires, Marcelo T. de Alvear 2142, 1122AAH, Buenos Aires, Argentina.
Arch Oral Biol. 2002 Oct;47(10):717-22. doi: 10.1016/s0003-9969(02)00057-2.
It is not known whether the mechanisms involved in amylase release in submandibular and parotid glands are similar. Here, the participation of different signalling pathways in amylase release by the parotid and submandibular glands of the male rat was compared by studying the secretory response after beta-adrenergic stimulation. The beta-adrenergic agonist isoproterenol induced an increase of cAMP in both salivary glands, but while in the parotid it triggered amylase release, in the submandibular it was unable to increase amylase secretion. Parotid amylase release was dependent on adenylate cyclase activation, as SQ-22536 inhibited the secretory effect. In contrast, submandibular amylase secretion did not depend on the intracellular concentration of cAMP, as SQ-22536 did not modify its secretory response. Moreover, other activators of adenylate cyclase, such as forskolin and prostaglandin E2, also failed to modify amylase release by the submandibular gland. Neither ionophores nor calcium-blocking agents, as well as calcium-calmodulin and nitric oxide synthase inhibitors, were effective in modifying basal amylase release by the submandibular gland. However, the disruption of microfilaments with cytochalasin B, but not the disruption of microtubules with colchicine, prevented amylase release in that gland. It is concluded that amylase exocytosis in the submandibular gland is a constitutive non-regulated phenomenon, as it is independent of extracellular or intracellular signals. It depends only on the integrity of the microfilaments, probably used by the vesicles to travel from the Golgi apparatus to the plasma membrane.
目前尚不清楚下颌下腺和腮腺中淀粉酶释放所涉及的机制是否相似。在此，通过研究β-肾上腺素能刺激后的分泌反应，比较了不同信号通路在雄性大鼠腮腺和下颌下腺淀粉酶释放中的参与情况。β-肾上腺素能激动剂异丙肾上腺素可使两种唾液腺中的cAMP增加，但在腮腺中它引发淀粉酶释放，而在下颌下腺中它无法增加淀粉酶分泌。腮腺淀粉酶释放依赖于腺苷酸环化酶的激活，因为SQ-22536抑制了分泌效应。相比之下，下颌下腺淀粉酶分泌不依赖于细胞内cAMP浓度，因为SQ-22536未改变其分泌反应。此外，腺苷酸环化酶的其他激活剂，如福斯可林和前列腺素E2，也未能改变下颌下腺的淀粉酶释放。离子载体、钙阻滞剂以及钙调蛋白和一氧化氮合酶抑制剂均不能有效改变下颌下腺的基础淀粉酶释放。然而，用细胞松弛素B破坏微丝，但用秋水仙碱破坏微管则不能阻止该腺体中的淀粉酶释放。得出的结论是，下颌下腺中的淀粉酶胞吐是一种组成性非调节现象，因为它独立于细胞外或细胞内信号。它仅取决于微丝的完整性，微丝可能被囊泡用于从高尔基体运输到质膜。
