Reference : Multiple muscarinic receptor subtypes mediating pulmonary oedema in the rabbit.
Scientific journals : Article
Life sciences : Veterinary medicine & animal health
Human health sciences : Pharmacy, pharmacology & toxicology
Multiple muscarinic receptor subtypes mediating pulmonary oedema in the rabbit.
Delaunois, Annie mailto [Université de Liège - ULiège > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire >]
Gustin, Pascal mailto [Université de Liège - ULiège > Département de sciences fonctionnelles > Pharmacologie, pharmacothérapie et toxicologie >]
Ansay, Michel mailto [Université de Liège - ULiège > Services généraux (Faculté de médecine vétérinaire) > Relations académiques et scientifiques (Méd. vétérinaire) >]
Pulmonary Pharmacology
Academic Press
Yes (verified by ORBi)
United Kingdom
[en] Acetylcholine/physiology ; Animals ; Capsaicin ; Female ; Lung/innervation ; Male ; Muscarinic Antagonists/pharmacology ; Nerve Fibers/physiology ; Neuropeptides/secretion ; Pulmonary Edema/chemically induced/physiopathology ; Rabbits ; Receptors, Muscarinic/classification/physiology
[en] The effects of various muscarinic antagonists on acetylcholine (ACh)-induced pulmonary oedema were studied in isolated perfused rabbit lungs. ACh induced a dose-dependent increase in the capillary filtration coefficient (Kf,c). This effect has been previously related to the activation of the capsaicin-sensitive nerve fibres and the release of substance P. Atropine, pirenzepine (M1-selective antagonist) and 4-DAMP (M3-selective antagonist) altered this response, producing a dose-dependent shift to the right of the ACh concentration-Kf,c response curve. By contrast, the M2-selective antagonist AFDX-116 shifted the ACh concentration-response curve to the left. Atropine, pirenzepine and 4-DAMP also significantly reduced the capsaicin-induced increase in the Kf,c, while AFDX-116 enhanced it. We conclude that multiple muscarinic receptor subtypes are present in the rabbit lung, located on the C-fibres, and are involved in the ACh-induced pulmonary oedema. M1 and M3 receptors seem to stimulate the release of neuropeptides from C-fibres, whereas M2 receptors have an inhibitory effect on these fibers.
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