首页> 外文期刊>Life sciences >Galanin and somatostatin inhibition of neurokinin A and B induced airway mucus secretion in the rat.
【24h】

Galanin and somatostatin inhibition of neurokinin A and B induced airway mucus secretion in the rat.

机译:甘丙肽和生长抑素抑制神经激肽A和B诱导大鼠气道粘液分泌。

获取原文
获取原文并翻译 | 示例
获取外文期刊封面目录资料

摘要

Neurokinin A and B are present in neurons situated in lung and NK-1 receptors have been described on tracheal submucosal gland cells. In the present study we compared the ability of substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) to stimulate airway mucus secretion. Furthermore, we characterized the interaction of NKA and NKB with galanin and somatostatin. The rank order of the tachykinins to stimulate airway mucus secretion was SP > NKA > NKB suggesting that NK-1 receptors mediate these effects(EC50:SP: 50 nmol/l, NKA: 200 nmol/l, NKB: 400 nmol/l). Galanin and somatostatin were equally potent to inhibit NK-A and NK-B stimulated airway mucus release. These results suggest that NK-A and NK-B are potent stimulators of airway macromolecule secretion. Galanin and somatostatin potently inhibit these actions of the tachykinins. Therefore, airway mucus secretion is controlled by a complex network of several different mediators.
机译:神经激肽A和B存在于位于肺中的神经元中,并且已经在气管粘膜下腺细胞上描述了NK-1受体。在本研究中,我们比较了物质P(SP),神经激肽A(NKA)和神经激肽B(NKB)刺激气道粘液分泌的能力。此外,我们表征了NKA和NKB与甘丙肽和生长抑素的相互作用。速激肽刺激气道粘液分泌的顺序为SP> NKA> NKB,表明NK-1受体介导了这些作用(EC50:SP:50 nmol / l,NKA:200 nmol / l,NKB:400 nmol / l) 。甘丙肽和生长抑素同样有效地抑制NK-A和NK-B刺激的气道粘液释放。这些结果表明,NK-A和NK-B是气道大分子分泌的有效刺激剂。甘丙肽和生长抑素有效抑制速激肽的这些作用。因此,气道粘液分泌受几种不同介体的复杂网络控制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号