scholarly journals Role of Parasympathetic Nerves and Muscarinic Receptors in Allergy and Asthma

2012 ◽  
pp. 48-69 ◽  
Author(s):  
Gregory D. Scott ◽  
Allison D. Fryer
Keyword(s):  
Muscarinic Receptors ◽  
Parasympathetic Nerves ◽  
Allergy And Asthma

Insulin sensitivity is mediated by the activation of the ACh/NO/cGMP pathway in rat liver

2004 ◽  
Vol 287 (3) ◽  
pp. G527-G532 ◽  
Author(s):  
Maria P. Guarino ◽  
Nina C. Correia ◽  
W. Wayne Lautt ◽  
M. Paula Macedo
Keyword(s):  
Nitric Oxide ◽  
Insulin Sensitivity ◽  
Muscarinic Receptors ◽  
Wistar Rats ◽  
No Donor ◽  
Parasympathetic Nerves ◽  
Cgmp Pathway ◽  
Male Wistar Rats ◽  
Oxide Synthase

The hepatic parasympathetic nerves and hepatic nitric oxide synthase (NOS) are involved in the secretion of a hepatic insulin sensitizing substance (HISS), which mediates peripheral insulin sensitivity. We tested whether binding of ACh to hepatic muscarinic receptors is an upstream event to the synthesis of nitric oxide (NO), which, along with the activation of hepatic guanylate cyclase (GC), permits HISS release. Male Wistar rats (8–9 wk) were anesthetized with pentobarbital sodium (65 mg/kg). Insulin sensitivity was assessed using a euglycemic clamp [the rapid insulin sensitivity test (RIST)]. HISS inhibition was induced by antagonism of muscarinic receptors (atropine, 3 mg/kg iv) or by blockade of NOS [ NG-nitro-l-arginine methyl ester (l-NAME), 1 mg/kg intraportally (ipv)]. After the blockade, HISS action was tentatively restored using a NO donor [3-morpholynosydnonimine (SIN-1), 5–10 mg/kg ipv] or ACh (2.5–5 μg·kg−1·min−1 ipv). SIN-1 (10 mg/kg) reversed the inhibition caused by atropine (RIST postatropine 137.7 ± 8.3 mg glucose/kg; reversed to 288.3 ± 15.5 mg glucose/kg, n = 6) and by l-NAME (RIST post-l-NAME 152.2 ± 21.3 mg glucose/kg; reversed to 321.7 ± 44.7 mg glucose/kg, n = 5). ACh did not reverse HISS inhibition induced by l-NAME. The role of GC in HISS release was assessed using 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 5 nmol/kg ipv), a GC inhibitor that decreased HISS action (control RIST 237.6 ± 18.6 mg glucose/kg; RIST post-ODQ 111.7 ± 6.2 mg glucose/kg, n = 5). We propose that hepatic parasympathetic nerves release ACh, leading to hepatic NO synthesis, which activates GC, triggering HISS action.

Ozone-induced hyperresponsiveness and blockade of M2 muscarinic receptors by eosinophil major basic protein

1999 ◽  
Vol 87 (4) ◽  
pp. 1272-1278 ◽  
Author(s):  
Bethany L. Yost ◽  
Gerald J. Gleich ◽  
Allison D. Fryer
Keyword(s):  
Muscarinic Receptors ◽  
Guinea Pigs ◽  
Basic Protein ◽  
Muscarinic Agonist ◽  
Receptor Function ◽  
Major Basic Protein ◽  
Interleukin 5 ◽  
Parasympathetic Nerves ◽  
Eosinophil Major Basic Protein

Control of airway smooth muscle is provided by parasympathetic nerves that release acetylcholine onto M3 muscarinic receptors. Acetylcholine release is limited by inhibitory M2 muscarinic receptors. In antigen-challenged guinea pigs, hyperresponsiveness is due to blockade of neuronal M2 receptors by eosinophil major basic protein (MBP). Because exposure of guinea pigs to ozone also causes M2dysfunction and airway hyperresponsiveness, the role of eosinophils in ozone-induced hyperresponsiveness was tested. Animals were exposed to filtered air or to 2 parts/million ozone for 4 h. Twenty-four hours later, the muscarinic agonist pilocarpine no longer inhibited vagally induced bronchoconstriction in ozone-exposed animals, indicating M2 dysfunction. M2 receptor function in ozone-exposed animals was protected by depletion of eosinophils with antibody to interleukin-5 and by pretreatment with antibody to guinea pig MBP. M2 function was acutely restored by removal of MBP with heparin. Ozone-induced hyperreactivity was also prevented by antibody to MBP and was reversed by heparin. These data show that loss of neuronal M2 receptor function after ozone is due to release of eosinophil MBP.

Role of Nicotinic and Muscarinic Receptors on Synaptic Plasticity and Neurological Diseases

2016 ◽  
Vol 22 (14) ◽  
pp. 2004-2014 ◽  
Author(s):  
Marco Fuenzalida ◽  
Miguel Ángel Pérez ◽  
Hugo R. Arias
Keyword(s):  
Synaptic Plasticity ◽  
Muscarinic Receptors ◽  
Neurological Diseases

THE ROLE OF BRAIN STEM MUSCARINIC RECEPTORS IN THE REGULATION OF BREATHING

1996 ◽  
Author(s):  
Βασιλική Μάλλιου
Keyword(s):  
Brain Stem ◽  
Muscarinic Receptors ◽  
In Vitro Autoradiography ◽  
Regulation Of Breathing

ΧΟΛΙΝΕΡΓΙΚΟΙ ΜΗΧΑΝΙΣΜΟΙ ΠΑΙΖΟΥΝ ΣΗΜΑΝΤΙΚΟ ΡΟΛΟ ΣΤΟΝ ΕΛΕΓΧΟ ΤΗΣ ΑΝΑΠΝΟΗΣ, ΑΛΛΑ Η ΚΑΤΑΝΟΜΗ ΤΩΝ ΜΟΥΣΚΑΡΙΝΙΚΩΝ ΧΟΛΙΝΕΡΓΙΚΩΝ ΥΠΟΔΟΧΕΩΝ ΔΕΝ ΕΧΟΥΝ ΧΑΡΤΟΓΡΑΦΗΘΕΙ ΣΤΑ ΑΝΑΠΝΕΥΣΤΙΚΑ ΚΕΝΤΡΑ ΤΟΥ ΣΤΕΛΕΧΟΥ ΤΟΥ ΕΓΚΕΦΑΛΟΥ. ΤΟ ΠΡΩΤΟ ΜΕΡΟΣ ΤΗΣ ΠΑΡΟΥΣΑΣ ΕΡΓΑΣΙΑΣ ΕΞΕΤΑΣΕ ΤΗΝ ΥΠΟΘΕΣΗ ΟΤΙ ΥΠΑΡΧΕΙ ΕΤΕΡΟΓΕΝΗ ΚΑΤΑΝΟΜΗ MACHR ΥΠΟΔΟΧΕΩΝ ΣΤΑ ΑΝΑΠΝΕΥΣΤΙΚΑ ΚΕΝΤΡΑ. ΧΡΗΣΙΜΟΠΟΙΗΘΗΚΕ Η ΜΕΘΟΔΟΣ IN VITRO AUTORADIOGRAPHY ΓΙΑΤΗΝ ΠΟΣΟΤΙΚΗ ΚΑΙ ΠΟΙΟΤΙΚΗ ΚΑΤΑΝΟΜΗ ΤΩΝ ΥΠΟΔΟΧΕΩΝ ΣΤΑ ΑΝΑΠΝΕΥΣΤΙΚΑ ΚΕΝΤΡΑ. Η ΔΙΑΤΡΙΒΗ ΕΔΕΙΞΕ ΓΙΑ ΠΡΩΤΗ ΦΟΡΑ ΟΤΙ ΣΤΑ ΑΝΑΠΝΕΥΣΤΙΚΑ ΚΕΝΤΡΑ ΤΟΥ ΕΓΚΕΦΑΛΟΥ ΥΠΑΡΧΕΙ ΕΤΕΡΟΓΕΝΗ ΚΑΤΑΝΟΜΗ MACHR ΥΠΟΔΟΧΕΩΝ. ΕΤΣΙ ΣΤΑ ΑΠΟΤΕΛΕΣΜΑΤΑ ΤΗΣ ΠΑΡΟΥΣΑΣ ΕΡΓΑΣΙΑΣ ΕΙΝΑΙ ΟΥΣΙΑΣΤΙΚΟ ΠΡΩΤΟ ΒΗΜΑ ΓΙΑ ΜΕΛΛΟΝΤΙΚΕΣ ΕΡΓΑΣΙΕΣ ΜΕ ΣΤΟΧΟ ΝΑ ΔΙΕΥΚΡΙΝΙΣΤΕΙ Ο ΛΕΙΤΟΥΡΓΙΚΟΣ ΡΟΛΟΣ ΤΩΝ MACHR ΥΠΟΔΟΧΕΩΝ ΤΟΥ ΣΤΕΛΕΧΟΥ ΣΤΟΝ ΕΛΕΓΧΟ ΤΗΣ ΑΝΑΠΝΟΗΣ. ΤΟ ΔΕΥΤΕΡΟ ΜΕΡΟΣ ΤΗΣ ΔΙΑΤΡΙΒΗΣ ΕΞΕΤΑΣΕ ΤΗΝ ΔΡΑΣΗ ΤΟΥ ΜΟΥΣΚΑΡΙΝΙΚΟΥ ΑΓΩΝΙΣΤΗ BETH ΚΑΙ ΤΩΝ ΜΟΥΣΚΑΡΙΝΙΚΩΝ ΑΝΤΑΓΩΝΙΣΤΩΝ 4-DAMP ΚΑΙ METHATRAMINE ΣΤΗΝ ΑΝΑΠΝΕΥΣΤΙΚΗ ΣΥΧΝΟΤΗΤΑ (AL) ΚΑΤΑ ΤΗ ΔΙΑΡΚΕΙΑ NREM ΚΑΙ REM ΥΠΝΟΥ. Η ΕΡΓΑΣΙΑ ΕΔΕΙΞΕ ΟΤΙ Η BETH ΣΤΟ MPRF ΤΟΥ ΣΤΕΛΕΧΟΥ ΠΡΟΚΑΛΕΙ ΜΕΙΩΣΗ ΤΗΣ ΑΣ (P < 0.05) ΚΑΤΑ NREMΚΑΙ REM ΥΠΝΟΥ. ΜΙΚΡΟΕΓΧΥΣΕΙΣ 4-DAMP ΚΑΙ METH ΧΡΗΣΙΜΟΠΟΙΗΘΗΚΑΝ ΓΙΑ ΤΗΝ ΕΞΕΤΑΣΗΤΗΣ ΥΠΟΘΕΣΗΣ ΟΤΙ Η ΜΕΙΩΣΗ ΤΗΣ ΑΣ ΔΕΝ ΜΠΟΡΕΙ ΝΑ ΞΕΧΩΡΙΣΤΕΙ ΑΠΟ ΤΟ ΣΤΑΔΙΟ ΕΓΡΗΓΟΡΣΗΣ. Η ΕΡΓΑΣΙΑ ΑΥΤΗ ΕΔΕΙΞΕ ΓΙΑ ΠΡΩΤΗ ΦΟΡΑ ΟΤΙ ΟΙ ΜΟΥΣΚΑΡΙΝΙΚΟΙ ΑΝΤΑΓΩΝΙΣΤΕΣ 4-DAMP ΚΑΙ METH ΔΕΝ ΕΜΠΟΔΙΣΑΝ ΤΗΝ ΜΕΙΩΣΗ ΤΗΣ ΑΣ ΠΟΥ ΣΥΝΟΔΕΥΕΙ ΤΟ ΣΤΑΔΙΟ ΕΓΡΗΓΟΡΣΗΣ.

Dysfunction of M2-muscarinic receptors in pulmonary parasympathetic nerves after antigen challenge

1991 ◽  
Vol 71 (6) ◽  
pp. 2255-2261 ◽  
Author(s):  
A. D. Fryer ◽  
M. Wills-Karp
Keyword(s):  
Muscarinic Receptors ◽  
Guinea Pigs ◽  
Antigen Challenge ◽  
Saline Control ◽  
Control Group ◽  
Vagus Nerves ◽  
Parasympathetic Nerves ◽  
Volume Blood ◽  
M2 Muscarinic Receptors ◽  
Stimulation Of

The effect of antigen challenge on the function of neuronal M2-muscarinic autoreceptors in the lungs was studied in anesthetized guinea pigs. Guinea pigs were injected intraperitoneally with saline (control group) or ovalbumin (10 mg/kg) on days 1, 3, and 5. One group of sensitized animals was challenged on days 20–25 with aerosolized ovalbumin for 5 min/day (challenged group), while another group of the sensitized animals was not challenged (sensitized group). On day 26 the animals were anesthetized, paralyzed, tracheostomized, and artificially ventilated. Pulmonary inflation pressure (Ppi), tidal volume, blood pressure, and heart rate were recorded. Both vagus nerves were cut, and electrical stimulation of the distal portions caused bronchoconstriction (measured as an increase in Ppi) and bradycardia. In the control group, pilocarpine (1–100 micrograms/kg iv) attenuated vagally induced bronchoconstriction by stimulating inhibitory M2-muscarinic receptors on parasympathetic nerves in the lungs. Conversely, blockade of these receptors with the antagonist gallamine (0.1–10 mg/kg iv) produced a marked potentiation of vagally induced bronchoconstriction. These results confirm previous findings. In the challenged guinea pigs, pilocarpine did not inhibit vagally induced bronchoconstriction. Furthermore, gallamine did not potentiate vagally induced bronchoconstriction to the same degree as in the controls. In the group of animals that was sensitized but not challenged, the potentiation of vagally induced bronchoconstriction by gallamine was identical to the controls. There was no increase in baseline Ppi in the sensitized or challenged animals compared with the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Neuromuscular Relaxants as Antagonists for M2and M3Muscarinic Receptors 

1998 ◽  
Vol 88 (3) ◽  
pp. 744-750 ◽  
Author(s):  
Vivian Y. Hou ◽  
Carol A. Hirshman ◽  
Charles W. Emala
Keyword(s):  
Muscarinic Receptor ◽  
Muscarinic Receptors ◽  
Radioligand Binding ◽  
Chinese Hamster ◽  
Neuromuscular Relaxants ◽  
Ovary Cell ◽  
Relative Order ◽  
Parasympathetic Nerves ◽  
M2 Muscarinic Receptor ◽  
M3 Muscarinic Receptor

Background Neuromuscular relaxants such as pancuronium bind to M2 and M3 muscarinic receptors as antagonists. Blockade of muscarinic receptors in atria of the M2 subtype mediates tachycardia. In the lung, blockade of M2 receptors on parasympathetic nerves potentiates vagally induced bronchospasm, whereas blockade of M3 receptors on bronchial smooth muscle inhibits bronchospasm. The current study was designed to quantify the affinity of a series of neuromuscular relaxants for the M2 and M3 muscarinic receptors, which were individually stably transfected in Chinese hamster ovary cell lines. Methods Competitive radioligand binding assays determined the relative binding affinities of the neuromuscular relaxants pancuronium, succinylcholine, mivacurium, doxacurium, atracurium, rocuronium, gallamine, and pipecuronium for the muscarinic receptor in the presence of a muscarinic receptor antagonist (3H-QNB) in membranes prepared from cells individually expressing either the M2 or M3 muscarinic receptor. Results All muscle relaxants evaluated displaced 3H-QNB from muscarinic receptors. The relative order of potency for the M2 muscarinic receptor (highest to lowest) was pancuronium, gallamine, rocuronium, atracurium, pipecuronium, doxacurium, mivacurium, and succinylcholine. The relative order of potency for the M3 muscarinic receptor (highest to lowest) was pancuronium, atracurium, pipecuronium, rocuronium, mivacurium, gallamine, succinylcholine, and doxacurium. Conclusions All neuromuscular relaxants studied had affinities for the M2 and M3 muscarinic receptor, but only pancuronium and gallamine had affinities within the range of concentrations achieved with clinical use. The high affinities of gallamine and pancuronium for the M2 muscarinic receptor are consistent with a mechanism of M2 receptor blockade in relaxant-induced tachycardia.

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