Endogenous noradrenaline release from guinea‐pig isolated trachea is inhibited by activation of M₂ receptors

Abstract

Overflow of endogenous noradrenaline (NA) from guinea-pig isolated tracheae was evoked by electrical field stimulation (3 Hz, 540 pulses). The muscarinic receptor agonist oxotremorine inhibited the evoked overflow of NA in a concentration-dependent manner (EC" 84 nM). Methoctramine, pirenzepine and p-fluoro-hexahydrosiladiphenidol (each 1 pM) shifted the concentration-response curves of oxotremorine to the right with apparent pA2 values of 7.60, 6.74 and 6.18, respectively. It is concluded that sympathetic nerve terminals in the guinea-pig trachea are endowed with inhibitory muscarinic M2 receptors.

Insulin Regulates Neuronal M2Muscarinic Receptor Function in the Ileum of Diabetic Rats

“…This increase may be due in part to inhibition of neuronal M 2 muscarinic receptors. M 2 muscarinic receptors have been localized to sympathetic nerves where they limit noradrenaline release (Racke et al, 1992;Yokotani and Osumi, 1993;Lambrecht et al, 1999). Thus, inhibition of M 2 muscarinic receptor function by insulin would lead to increased noradrenaline release.…”

Pancuronium masks the prejunctional muscarinic autoreceptor in guinea pig tracheal smooth muscle

“…Since EFS-induced contractions were completely blocked by the muscarinic antagonist atropine (bath concentration: 1 pM) and not influenced by the nicotinergic ganglion blocking drug hexamethonium (bath concentration: 10 pM), it may be concluded that the EFS-induced contraction with parameters as described, is mainly due to postganglionic, cholinergic stimulation. However, guinea-pig tracheal smooth muscles receive a dual innervation from both the parasympathetic and sympathetic nervous system and evidence exist for cross talk between the two neuronal systems (14)(15)(16).…”