Altered distribution of M2 and M4 muscarinic receptor expression in vitiligo

2010 ◽  
Vol 38 (5) ◽  
pp. 493-497
Author(s):  
Sirintip CHAICHALOTORNKUL ◽  
Montree UDOMPATAIKUL ◽  
Udomsri SHOWPITTAPORNCHAI ◽  
Piti PALUNGWACHIRA ◽  
Wisuit PRADIDARCHEEP
2010 ◽  
Vol 79 (2) ◽  
pp. 251-261 ◽  
Author(s):  
Erica Rosemond ◽  
Mario Rossi ◽  
Sara M. McMillin ◽  
Marco Scarselli ◽  
Julie G. Donaldson ◽  
...  

2014 ◽  
Vol 86 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Douglas A. Schober ◽  
Carrie H. Croy ◽  
Hongling Xiao ◽  
Arthur Christopoulos ◽  
Christian C. Felder

2018 ◽  
Vol 199 (4S) ◽  
Author(s):  
Mehmet Kazim Asutay ◽  
Banu Aydin ◽  
Hasan Toper ◽  
Deniz Filinte ◽  
Hülya Cabadak ◽  
...  

2009 ◽  
Vol 2009 ◽  
pp. 1-6
Author(s):  
Anders T. Ryberg ◽  
Ondrej Soukup ◽  
Gunnar Tobin

In the in vivo experiments on anaesthetized sheep, it was presently examined whether muscarinic receptor antagonists with diverse selectivity affect the release of VIP in response to electrical stimulation of the parasympathetic chorda tympanic nerve differently, and if the changes in the release could be associated to altered secretory and vasodilator responses. The location of the muscarinic receptor subtypes was examined also. In the experiments, blood was collected out of the submandibular venous drainage before and during electrical stimulation of chorda tympani nerve in the absence and presence either of pirenzepine or methoctramine. While metchoctramine increased the output of protein, pirenzepine inhibited flow of saliva and increased protein output, vasodilatation, and VIP output. In morphological examinations, the inhibitory muscarinic M4 receptor occurred interacinarily in the gland. It is concluded that prejunctional muscarinic receptors, most likely of the M4 subtype, exert inhibitory modulation of the parasympathetic release of VIP in the ovine submandibular gland.


1995 ◽  
Vol 268 (6) ◽  
pp. L935-L940 ◽  
Author(s):  
C. W. Emala ◽  
A. Aryana ◽  
M. A. Levine ◽  
R. P. Yasuda ◽  
S. A. Satkus ◽  
...  

Airway smooth muscle from asthmatic humans and from the Basenji-greyhound dog (BG) dog is hyporesponsive to beta-adrenergic agonist stimulation. Because adenylyl cyclase is under dual regulation in airway smooth muscle, we compared muscarinic receptor-coupled inhibition of adenylyl cyclase in airway smooth muscle from BG and mongrel dogs. Inhibition of forskolin-stimulated adenylyl cyclase activity by the muscarinic M2 agonist oxotremorine was greater in airway smooth muscle membranes from BG compared with mongrel controls. Quantitative immunoprecipitation studies showed increased numbers of m2 but not m3 muscarinic receptors in the BG airway smooth muscle. The enhanced ability of muscarinic agonists to inhibit adenylyl cyclase in BG airway smooth muscle may be due to the greater numbers of muscarinic m2 receptors, which may account in part for impaired airway smooth muscle relaxation in the BG model of airway hyperresponsiveness.


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