Shimura S, Sasaki T, Ikeda K, Sasaki H, Takishima T
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
J Appl Physiol (1985). 1988 Dec;65(6):2537-44. doi: 10.1152/jappl.1988.65.6.2537.
Using isolated submucosal glands from feline trachea, we examined the effect of vasoactive intestinal peptide (VIP) on mucus glycoprotein secretion and glandular contraction by measuring released radiolabeled glycoconjugates and induced tension, respectively. VIP (10(-10) to 10(-6) M) produced a dose-dependent increase in [3H]glycoconjugate release of up to 300% of controls, which was inhibited by VIP antiserum and not inhibited by atropine, propranolol, or phentolamine. VIP at a low concentration (10(-9) M), which did not produce any significant increases over controls, produced a 2.4- to 5-fold augmentation of the glycoconjugate release induced by 10(-9) to 10(-7) M methacholine (MCh). Atropine or VIP antiserum abolished the augmentation. VIP did not produce any alteration in isoproterenol- or phenylephrine-evoked glycoconjugate secretion. VIP (up to 10(-5) M) did not produce any alteration in the tension, even when the gland had contracted with MCh, or any augmentation of contraction induced by MCh (10(-9) to 10(-7) M). These results indicate that VIP induces mucus glycoprotein release from secretory cells and also that it potentiates the secretion induced by cholinergic stimulation.
我们使用猫气管分离出的粘膜下腺,分别通过测量释放的放射性标记糖缀合物和诱导张力,研究了血管活性肠肽(VIP)对粘液糖蛋白分泌和腺体收缩的影响。VIP(10^(-10)至10^(-6) M)使[3H]糖缀合物释放呈剂量依赖性增加,最高可达对照的300%,这被VIP抗血清抑制,而阿托品、普萘洛尔或酚妥拉明未抑制。低浓度(10^(-9) M)的VIP未使释放量相比对照有任何显著增加,但使10^(-9)至10^(-7) M的乙酰甲胆碱(MCh)诱导的糖缀合物释放增加了2.4至5倍。阿托品或VIP抗血清消除了这种增强作用。VIP对异丙肾上腺素或去氧肾上腺素诱发的糖缀合物分泌没有产生任何改变。即使腺体已被MCh收缩,高达10^(-5) M的VIP也未使张力产生任何改变,或增强MCh(10^(-9)至10^(-7) M)诱导的收缩。这些结果表明,VIP诱导分泌细胞释放粘液糖蛋白,并且还增强胆碱能刺激诱导的分泌。