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甘丙肽和生长抑素对大鼠中神经激肽A和B诱导的气道黏液分泌的抑制作用。

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

作者信息

Wagner U, Fehmann H C, Bredenbröker D, Yu F, Barth P J, von Wichert P

机构信息

Department of Internal Medicine, Philipps-University of Marburg, Germany.

出版信息

Life Sci. 1995;57(3):283-9. doi: 10.1016/0024-3205(95)00271-7.

Abstract

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.

摘要

神经激肽A和B存在于位于肺部的神经元中,并且在气管黏膜下腺细胞上已发现有NK-1受体。在本研究中,我们比较了P物质(SP)、神经激肽A(NKA)和神经激肽B(NKB)刺激气道黏液分泌的能力。此外,我们还对NKA和NKB与甘丙肽和生长抑素的相互作用进行了表征。速激肽刺激气道黏液分泌的强度顺序为SP > NKA > NKB,这表明NK-1受体介导了这些效应(半数有效浓度:SP为50 nmol/L,NKA为200 nmol/L,NKB为400 nmol/L)。甘丙肽和生长抑素在抑制NKA和NKB刺激的气道黏液释放方面具有同等效力。这些结果表明,NK-A和NK-B是气道大分子分泌的有效刺激物。甘丙肽和生长抑素能有效抑制速激肽的这些作用。因此,气道黏液分泌受几种不同介质组成的复杂网络控制。

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