Shimura S, Sasaki T, Ikeda K, Ishihara H, Sato M, Sasaki H, Takishima T
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Am Rev Respir Dis. 1991 Mar;143(3 Pt 2):S25-7. doi: 10.1164/ajrccm/143.3_Pt_2.S25.
Our study using feline tracheal isolated submucosal gland preparation has revealed that substance P (SP) produces an increase in submucosal gland secretion through the actions of both mucus ejection by glandular contraction and macromolecule secretion from secretory cells, and that the two actions are both mediated by a peripheral cholinergic action. In contrast, SP has no significant effect on macromolecule secretion from secretory cells in tracheal explants, probably because of epithelial suppression. Our study using an isolated gland preparation has also indicated that VIP potentiates mucous glycoprotein secretion induced by cholinergic stimulation through an interaction between muscarinic and VIP receptors in secretory cells. However, VIP failed to induce any significant glandular contraction or relaxation, indicating a lack of VIP receptors or a difference in the subtypes of muscarinic receptors in myoepithelial cells in submucosa glands.
我们利用猫气管分离黏膜下腺制备物进行的研究表明,P物质(SP)通过腺收缩导致的黏液排出和分泌细胞的大分子分泌这两种作用,使黏膜下腺分泌增加,且这两种作用均由外周胆碱能作用介导。相比之下,SP对气管外植体分泌细胞的大分子分泌无显著影响,这可能是由于上皮抑制所致。我们利用分离腺体制备物进行的研究还表明,血管活性肠肽(VIP)通过分泌细胞中毒蕈碱受体和VIP受体之间的相互作用,增强胆碱能刺激诱导的黏液糖蛋白分泌。然而,VIP未能诱导任何显著的腺体收缩或舒张,这表明黏膜下腺肌上皮细胞中缺乏VIP受体或毒蕈碱受体亚型存在差异。