The effect has been studied of sodium cromoglycate (SCG) on the activity of ‘C’ fibre sensory nerve endings in the canine lung. Pretreatment with SCG (100 μg/kg i.v.) reduced the excitation of these endings by capsaicin (10 μg/kg i.v.) for approximately 45 min. This property of SCG may explain its ability to suppress certain types of bronchoconstrictor responses in man.
SUIMMARY1. The ability of histamine, acetylcholine (ACh) and 5-hydroxytryptamine (5-HT) given i.v. and by aerosol to induce reflex bronchoconstriction and to activate lung irritant receptors has been studied in dogs anaesthetized with chloralose. 4. Histamine, 5-HT and ACh given by aerosol and i.v. increased lung irritant receptor discharge. Irrespective of the route of administration, for a given change in RL histamine produced a greater increase in irritant receptor discharge than did ACh or 5-HT, which produced similar increases.5. For a given change in RL, histamine, ACh and 5-HT were more effective in activating lung irritant receptors when given I.v. than by aerosol.6. The mechanisms of irritant receptor activation by histamine, ACh and 5-HT and the relationship between irritant receptor discharge and reflex bronchoconstriction are discussed.
1 Opioid receptors have been demonstrated on sensory fibres in the vagus nerve. Non-cholinergic (NC) neural bronchoconstriction in guinea-pig is due to release of neuropeptides from sensory nerve endings. We have therefore studied the effect of opioids on this NC bronchoconstriction in the anaesthetized guinea-pig. 2 Bilateral vagal stimulation (5 V, 5 ms, 10 Hz) caused reproducible bronchoconstriction in guineapigs which was reduced by atropine (1 mgkg 1), but the NC component was unaffected by hexamethonium (10 mg kg-1).3 NC bronchoconstriction was reduced by morphine in a dose-dependent manner (ED50= 132pgkg-1 with a maximal inhibition of 79 + 2.1% at 1 mgkg-1). Yohimbine (0.5 mgkg 1) did not alter the inhibitory effect of morphine (1 mg kg-1). 4 The inhibitory effect of morphine was completely reversed by naloxone (1 mg kg-1) which had no effect on NC bronchoconstriction. Propranolol (1 mg kg-1) significantly increased the NC bronchoconstrictor response but did not significantly alter the inhibition by morphine.5 The selective p-opioid receptor agonist Tyr-(D-Ala)-Gly-(N-Me-Phe)Glyol (DAGOL) was significantly more potent than morphine with an ED50 of 5.4pgkg-1 and complete inhibition at lOOgkg-. The 6-agonist Tyr4D-Pen)-Gly-Phe-D-Pen) (DPDPE) was less potent than DAGOL with an ED5o of 28pgkg-1 and a maximal inhibition of only 50 + 5% at lOOPgkg-. The Kreceptor agonist, U-50,488H had no inhibitory effect on the NC bronchoconstrictor response. 6 The bronchoconstrictor responses to exogenous substance P (25 pgkg-1) or acetylcholine (25 pg kg-1) were unaffected by morphine (500 pg kg-1). 7 We conclude that opioids inhibit the NC bronchoconstrictor response to vagal stimulation via an action on p-opioid receptors localized to sensory nerve endings in the airway.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.