Inhibitory and excitatory muscarinic receptors modulating the release of acetylcholine from the postganglionic parasympathetic neuron of the chicken heart

1992 ◽  
Vol 346 (4) ◽  
Author(s):  
G�nther Brehm ◽  
Ruth Lindmar ◽  
Konrad L�ffelholz
Keyword(s):  
Muscarinic Receptors ◽  
Chicken Heart ◽  
Release Of Acetylcholine ◽  
Parasympathetic Neuron

Ozone-induced airway hyperresponsiveness and loss of neuronal M2 muscarinic receptor function

1994 ◽  
Vol 76 (3) ◽  
pp. 1088-1097 ◽  
Author(s):  
A. H. Schultheis ◽  
D. J. Bassett ◽  
A. D. Fryer
Keyword(s):  
Muscarinic Receptor ◽  
Muscarinic Receptors ◽  
Ozone Exposure ◽  
Muscarinic Agonist ◽  
Receptor Function ◽  
Vagus Nerves ◽  
Parasympathetic Nerves ◽  
M2 Muscarinic Receptor ◽  
Release Of Acetylcholine ◽  
M2 Muscarinic Receptors

The effect of acute ozone exposure on the function of efferent parasympathetic nerves, M3 muscarinic receptors on airway smooth muscle, and inhibitory M2 muscarinic receptors on the parasympathetic nerves was studied. Immediately after exposure to 2.0 ppm ozone for 4 h, guinea pigs became hyperresponsive to electrical stimulation of the vagus nerves. The normal airway response to intravenous cholinergic agonists at this time demonstrates normal M3 receptor function. M2 muscarinic receptors on the nerves, which normally inhibit release of acetylcholine, were dysfunctional after ozone exposure, as demonstrated by the failure of the muscarinic agonist pilocarpine to inhibit, and the failure of the M2 antagonist gallamine to potentiate, vagally mediated bronchoconstriction. Thus, loss of inhibitory M2 muscarinic receptor function after ozone exposure potentiates release of acetylcholine from the vagus nerves, increasing vagally mediated bronchoconstriction. By 14 days, postozone responses to vagal nerve stimulation were not different from those of air-exposed animals and the function of the neuronal M2 muscarinic receptor was normal, confirming that ozone-induced hyperresponsiveness is reversible.

Interaction of enkephalin and caerulein on guinea pig small intestine

1983 ◽  
Vol 244 (1) ◽  
pp. G65-G70
Author(s):  
W. M. Yau ◽  
P. F. Lingle ◽  
M. L. Youther
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Muscarinic Receptors ◽  
Dose Response ◽  
Response Curve ◽  
Acetylcholine Release ◽  
Control Level ◽  
Release Studies ◽  
Release Of Acetylcholine

This is a report on the effect of caerulein and methionine-enkephalin interaction on mechanical contraction and acetylcholine release in vitro. The ability of enkephalin to relax caerulein-induced contractions and the manner in which the caerulein dose-response curve was shifted in the presence of enkephalin strongly suggest that enkephalin and caerulein are functional antagonists in this system. The failure of enkephalin to alter the action of exogenous acetylcholine implies that such an antagonism is not mediated through a competition with postsynaptic muscarinic receptors on the muscle. Data from acetylcholine-release studies indicate that caerulein stimulation was dose related. As with the mechanical contractions, the release of acetylcholine in response to caerulein was inhibited by enkephalin. However, naloxone was capable of blocking this inhibition and restoring the release to its control level without interfering with caerulein stimulation. These data provide evidence for the modulatory roles of neuronal peptides in the cholinergic control of gut motility.

A Mechanism for Rapacuronium-induced Bronchospasm

2003 ◽  
Vol 98 (4) ◽  
pp. 906-911 ◽  
Author(s):  
Edmund Jooste ◽  
Farrah Klafter ◽  
Carol A. Hirshman ◽  
Charles W. Emala
Keyword(s):  
Smooth Muscle ◽  
Muscarinic Receptor ◽  
Airway Smooth Muscle ◽  
Muscarinic Receptors ◽  
Radioligand Binding ◽  
Neuromuscular Blocking ◽  
Parasympathetic Nerve ◽  
Release Of Acetylcholine ◽  
M3 Muscarinic Receptor ◽  
M2 Muscarinic Receptors

Background A safe and effective ultra-short-acting nondepolarizing neuromuscular blocking agent is required to block nicotinic receptors to facilitate intubation. Rapacuronium, which sought to fulfill these criteria, was withdrawn from clinical use due to a high incidence of bronchospasm resulting in death. Understanding the mechanism by which rapacuronium induces fatal bronchospasm is imperative so that newly synthesized neuromuscular blocking agents that share this mechanism will not be introduced clinically. Selective inhibition of M2 muscarinic receptors by muscle relaxants during periods of parasympathetic nerve stimulation (e.g., intubation) can result in the massive release of acetylcholine to act on unopposed M3 muscarinic receptors in airway smooth muscle, thereby facilitating bronchoconstriction. Methods Competitive radioligand binding determined the binding affinities of rapacuronium, vecuronium, cisatracurium, methoctramine (selective M2 antagonist), and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP; selective M3 antagonist) for M2 and M3 muscarinic receptors. Results Rapacuronium competitively displaced 3H-QNB from the M2 muscarinic receptors but not from the M3 muscarinic receptors within clinically relevant concentrations. Fifty percent inhibitory concentrations (mean +/- SE) for rapacuronium were as follows: M2 muscarinic receptor, 5.10 +/- 1.5 microm (n = 6); M3 muscarinic receptor, 77.9 +/- 11 microm (n = 8). Cisatracurium and vecuronium competitively displaced 3H-QNB from both M2 and M3 muscarinic receptors but had affinities at greater than clinically achieved concentrations for these relaxants. Conclusions Rapacuronium in clinically significant doses has a higher affinity for M2 muscarinic receptors as compared with M3 muscarinic receptors. A potential mechanism by which rapacuronium may potentiate bronchoconstriction is by blockade of M2 muscarinic receptors on prejunctional parasympathetic nerves, leading to increased release of acetylcholine and thereby resulting in M3 muscarinic receptor-mediated airway smooth muscle constriction.

Cholinergic control of smooth muscle peristalsis in the cat esophagus

1989 ◽  
Vol 257 (4) ◽  
pp. G517-G523 ◽  
Author(s):  
E. L. Blank ◽  
B. Greenwood ◽  
W. J. Dodds
Keyword(s):  
Smooth Muscle ◽  
Synaptic Transmission ◽  
Muscarinic Receptors ◽  
Striated Muscle ◽  
Muscarinic Antagonist ◽  
Release Of Acetylcholine ◽  
High Doses ◽  
Secondary Peristalsis ◽  
M1 Muscarinic

The aim of this study was to examine in detail the effects of selective cholinergic and other pharmacological antagonists on primary and secondary peristalsis in the smooth muscle of the cat esophagus in order to fully characterize the cholinergic contribution to peristalsis in this species. Primary and secondary peristalsis in the smooth muscle part of the feline esophagus was completely abolished by atropine, 4-dephenylacetoxy-N-methylpiperidine methiodide (4-DAMP) (a selective M2 muscarinic antagonist), hexamethonium, and high doses of nicotine. Pirenzepine (a selective M1 muscarinic antagonist), propranolol, and phentolamine were without effect, as were naloxone, methysergide, and pyrilamine. From these findings we conclude that primary and secondary peristalsis in feline esophageal smooth muscle involves nicotinic ganglionic neurotransmission as well as postganglionic release of acetylcholine that acts directly on muscarinic receptors located on the smooth muscle. Peristalsis in esophageal striated muscle does not involve either synaptic transmission or muscarinic receptors.

1294: Quantitative Expression of Muscarinic Receptors in Urothelium and Detrusor of Healthy and Neurogenic Human Bladder

2006 ◽  
Vol 175 (4S) ◽  
pp. 417-417
Author(s):  
Shachi Tyagi ◽  
Naoki Yoshimura ◽  
Michael B. Chancellor ◽  
Fernando De Miguel
Keyword(s):  
Muscarinic Receptors ◽  
Human Bladder ◽  
Quantitative Expression
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