在从主动致敏豚鼠分离的气管中，β-内啡肽对过敏性收缩的上皮依赖性增强作用。

Epithelium-dependent potentiation of anaphylactic contractions by beta-endorphin in tracheae isolated from actively sensitized guinea-pigs.

作者信息

Van Oosterhout A J, Celeda L, Delsman K C, de Wied D, Nijkamp F P

机构信息

Department of Pharmacology, Faculty of Pharmacy, University of Utrecht, The Netherlands.

出版信息

Br J Pharmacol. 1991 Jun;103(2):1470-4. doi: 10.1111/j.1476-5381.1991.tb09813.x.

DOI:10.1111/j.1476-5381.1991.tb09813.x

PMID:1884103

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1908357/

Abstract

It has been shown that opioid peptides modulate airway function. In the present study, the effect of beta-endorphin on antigen-induced contractions of isolated tracheal rings from actively sensitized guinea-pigs has been studied. 2. beta-Endorphin had a concentration-dependent bimodal effect on anaphylactic contractions of the trachea. Low concentrations of beta-endorphin (10(-10) and 10(-8) M) significantly potentiated anaphylactic contractions, whereas higher concentrations (10(-7) and 10(-6) M) significantly suppressed anaphylactic contractions of guinea-pig trachea. 3. beta-Endorphin in concentrations of 10(-8) M and 10(-7) M did not affect the responsiveness of the tracheal rings to histamine or leukotriene D4. This indicates that beta-endorphin does not influence the responsiveness of tracheal smooth muscle to anaphylactic mediators. 4. In the presence of the non-selective opioid receptor antagonist naloxone, 10(-8) M beta-endorphin still potentiated the anaphylactic contractions of the trachea. In addition, an equimolar concentration of des-Tyr1-beta-endorphin, a fragment of beta-endorphin without opioid-like activity, also potentiated anaphylactic contractions. The potentiation of anaphylactic contraction by 10(-8) M beta-endorphin is not therefore mediated by classical opioid-receptors. 5. In the presence of naloxone, 10(-7) M, beta-endorphin did not suppress anaphylactic contractions of the trachea. Thus, the suppression of anaphylactic contraction is mediated via a classical opioid-receptor. 6. In epithelium-denuded trachea, both 10(-8) and 10(-7) M beta-endorphin suppressed the anaphylactic contractions, whereas 10(-8) and 10(-7) M des-Tyr1-beta-endorphin did not affect anaphylactic contractions. It is concluded that the potentiation of the anaphylactic contraction in intact trachea is epithelium-dependent whereas the suppression of the anaphylactic contraction is epithelium-independent.

摘要

已表明阿片肽可调节气道功能。在本研究中，研究了β-内啡肽对主动致敏豚鼠离体气管环抗原诱导收缩的影响。2. β-内啡肽对气管过敏收缩具有浓度依赖性的双峰效应。低浓度的β-内啡肽（10⁻¹⁰和10⁻⁸ M）显著增强过敏收缩，而较高浓度（10⁻⁷和10⁻⁶ M）则显著抑制豚鼠气管的过敏收缩。3. 10⁻⁸ M和10⁻⁷ M浓度的β-内啡肽不影响气管环对组胺或白三烯D4的反应性。这表明β-内啡肽不影响气管平滑肌对过敏介质的反应性。4. 在非选择性阿片受体拮抗剂纳洛酮存在下，10⁻⁸ Mβ-内啡肽仍能增强气管的过敏收缩。此外，等摩尔浓度的无阿片样活性的β-内啡肽片段去酪氨酸-β-内啡肽也能增强过敏收缩。因此，10⁻⁸ Mβ-内啡肽对过敏收缩的增强作用不是由经典阿片受体介导的。5. 在纳洛酮存在下，10⁻⁷ Mβ-内啡肽不抑制气管的过敏收缩。因此，过敏收缩的抑制是通过经典阿片受体介导的。6. 在去上皮的气管中，10⁻⁸和10⁻⁷ Mβ-内啡肽均抑制过敏收缩，而10⁻⁸和10⁻⁷ M去酪氨酸-β-内啡肽不影响过敏收缩。结论是，完整气管中过敏收缩的增强依赖于上皮，而过敏收缩的抑制不依赖于上皮。