Expression of neurokinin a receptor mRNA in human nasal mucosa

2004 ◽  
Vol 124 (sup553) ◽  
pp. 85-89 ◽  
Author(s):  
Hideaki Shirasaki ◽  
Etsuko Kanaizumi ◽  
Kazumasa Watanabe ◽  
Nobuhiro Konno ◽  
Jun Sato ◽  
...  
1991 ◽  
Vol 4 (3) ◽  
pp. 228-236 ◽  
Author(s):  
James N. Baraniuk ◽  
Jens D. Lundgren ◽  
Michiko Okayama ◽  
Julie Goff ◽  
Joaquim Mullol ◽  
...  

1992 ◽  
Vol 6 (4) ◽  
pp. 145-148 ◽  
Author(s):  
James N. Baraniuk ◽  
Michael A. Kaliner ◽  
Peter J. Barnes

Cholinergic nerves play an important part in the regulation of nasal secretions and nasal patency. In situ hybridization was used to identify the cells in human nasal mucosa that express the muscarinic m3 receptor mRNA, which codes for the M3 muscarinic receptor subtype protein. An m3 cDNA probe was biotin-labeled using terminal transferase and hybridized to tissue sections of formaldehyde- or formaldehyde/microwave irradiation-fixed human nasal mucosa. The biotinylated probe was detected using gold-labeled antibiotin antibodies with silver enhancement. Muscarinic m3 receptor mRNA was identified in all epithelial cells, both serous and mucous cells of submucosal glands, and endothelial cells of small muscular arteries, veins, and capillaries. This suggests that M3 receptors may mediate glandular secretion and vasomotor effects. M3-receptor antagonists active at these sites may reduce the glandular secretion and vasodilation that is produced by parasympathetic reflex activity in allergic and nonallergic rhinitis.


2003 ◽  
Vol 31 (3) ◽  
pp. 326-331 ◽  
Author(s):  
David A. Groneberg ◽  
Werner Heppt ◽  
Annette Cryer ◽  
Anke Wussow ◽  
Christian Peiser ◽  
...  

Author(s):  
Thi Nga Nguyen ◽  
Hideaki Suzuki ◽  
Jun-ichi Ohkubo ◽  
Tetsuro Wakasugi ◽  
Takuro Kitamura

<b><i>Background:</i></b> The ciliary beat of the airway epithelium, including the sinonasal epithelium, has a significant role in frontline defense and is thought to be controlled by the level of intracellular Ca<sup>2+</sup>. Involvement of calmodulin and adenylate/guanylate cyclases in the regulation of ciliary beats has been reported, and here we investigated the interrelation between these components of the ciliary beat regulatory pathway. <b><i>Methods:</i></b> The inferior turbinates were collected from 29 patients with chronic hypertrophic rhinitis/rhinosinusitis during endoscopic sinonasal surgery. The turbinate mucosa was cut into thin strips, and mucociliary movement was observed under a phase-contrast light microscope equipped with a high-speed digital video camera. <b><i>Results:</i></b> The ciliary beat frequency (CBF) was significantly increased by stimulation with 100 μM CALP3 (calmodulin agonist), which was completely suppressed by adding 100 µM SQ22536 (adenylate cyclase inhibitor) and 10 µM ODQ (guanylate cyclase inhibitor) together and by adding 1 µM KT5720 (protein kinase A inhibitor) and 1 µM KT5823 (protein kinase G inhibitor) together. The CBF was significantly increased by stimulation with 10 µM forskolin (adenylate cyclase activator) and 10 µM BAY41-2272 (guanylate cyclase activator) and by stimulation with 100 µM 8-bromo-cAMP (cAMP analog) and 100 µM 8-bromo-cGMP (cGMP analog), which was not changed by adding 1 µM calmidazolium (calmodulin antagonist). <b><i>Conclusions:</i></b> These results confirmed that the regulatory pathway of ciliary beats in the human nasal mucosa involves calmodulin, adenylate/guanylate cyclases, and protein kinases A/G and indicate that adenylate/guanylate cyclases and protein kinases A/G act downstream of calmodulin, but not vice versa, and that these cyclases relay calmodulin signaling.


1992 ◽  
Vol 89 (5) ◽  
pp. 1032-1039 ◽  
Author(s):  
J BARANIUK ◽  
P SILVER ◽  
M KALINER ◽  
P BARNES

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