Soluble guanylyl cyclase is localised in the acinar cells and participates in amylase secretion in rat parotid gland

It is well known that the muscarinic cholinergic agonists, carbachol and methacholine, enhance nitric oxide synthase (NOS) activity, and also stimulate salivary secretion. In the present study, we investigated whether salivary secretion by muscarinic cholinergic stimulation is mediated through the N...

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Published inArchives of oral biology Vol. 49; no. 9; pp. 691 - 696
Main Authors Shimomura, Hiromi, Tanaka, Satoshi, Komine, Nobuhiro, Shimooka, Shohachi, Imai, Akane, Nashida, Tomoko
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.09.2004
Subjects
Amylase
Amylases - analysis
Amylases - secretion
Animals
Carbachol - pharmacology
Cells, Cultured
cGMP
Cyclic GMP - analysis
Cyclic GMP - metabolism
Dentistry
Dose-Response Relationship, Drug
Enzyme Activators - pharmacology
Guanylate Cyclase - analysis
Guanylate Cyclase - antagonists & inhibitors
Guanylyl cyclase
Indazoles - pharmacology
Male
Muscarinic Agonists - pharmacology
Nitric Oxide - metabolism
Nitric Oxide Donors - pharmacology
Nitrogen oxide
Parotid Gland - drug effects
Parotid Gland - enzymology
Parotid Gland - secretion
Rat parotid gland
Rats
Rats, Wistar
S-Nitrosoglutathione - pharmacology
Signal Transduction - physiology
Nitrogen oxide
Rat parotid gland
Amylase
YC-1
cGMP
GSNO
ODQ
Guanylyl cyclase
sGC
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Abstract It is well known that the muscarinic cholinergic agonists, carbachol and methacholine, enhance nitric oxide synthase (NOS) activity, and also stimulate salivary secretion. In the present study, we investigated whether salivary secretion by muscarinic cholinergic stimulation is mediated through the NO/cGMP signaling pathway in rat salivary glands. Since NO activates soluble guanylyl cyclase (sGC) and cGMP may function as a mediator, the localisation of sGC was investigated in the salivary glands. sGC was localized in both the acinar and duct cells of the rat parotid and sublingual glands, and localized only in the acinar cells of the submandibular glands. S-Nitroso-glutathione (NO generator; GSNO) and YC-1 (NO-independent sGC activator) stimulated sGC in the cytosol to synthesise cGMP. The combination of GSNO and YC-1 stimulated sGC synergistically. Carbachol, GSNO and YC-1 enhanced amylase release from the rat parotid glands. Amylase release stimulated by carbachol and GSNO was inhibited by addition of the sGC inhibitor, ODQ, and cGMP-dependent protein kinase inhibitor, KT-5823. These results indicate that amylase release may be mediated through the NO/cGMP signaling pathway.
AbstractList It is well known that the muscarinic cholinergic agonists, carbachol and methacholine, enhance nitric oxide synthase (NOS) activity, and also stimulate salivary secretion. In the present study, we investigated whether salivary secretion by muscarinic cholinergic stimulation is mediated through the NO/cGMP signaling pathway in rat salivary glands. Since NO activates soluble guanylyl cyclase (sGC) and cGMP may function as a mediator, the localisation of sGC was investigated in the salivary glands. sGC was localized in both the acinar and duct cells of the rat parotid and sublingual glands, and localized only in the acinar cells of the submandibular glands. S-Nitroso-glutathione (NO generator; GSNO) and YC-1 (NO-independent sGC activator) stimulated sGC in the cytosol to synthesise cGMP. The combination of GSNO and YC-1 stimulated sGC synergistically. Carbachol, GSNO and YC-1 enhanced amylase release from the rat parotid glands. Amylase release stimulated by carbachol and GSNO was inhibited by addition of the sGC inhibitor, ODQ, and cGMP-dependent protein kinase inhibitor, KT-5823. These results indicate that amylase release may be mediated through the NO/cGMP signaling pathway.
It is well known that the muscarinic cholinergic agonists, carbachol and methacholine, enhance nitric oxide synthase (NOS) activity, and also stimulate salivary secretion. In the present study, we investigated whether salivary secretion by muscarinic cholinergic stimulation is mediated through the NO/cGMP signaling pathway in rat salivary glands. Since NO activates soluble guanylyl cyclase (sGC) and cGMP may function as a mediator, the localisation of sGC was investigated in the salivary glands. sGC was localized in both the acinar and duct cells of the rat parotid and sublingual glands, and localized only in the acinar cells of the submandibular glands. S-Nitroso-glutathione (NO generator; GSNO) and YC-1 (NO-independent sGC activator) stimulated sGC in the cytosol to synthesise cGMP. The combination of GSNO and YC-1 stimulated sGC synergistically. Carbachol, GSNO and YC-1 enhanced amylase release from the rat parotid glands. Amylase release stimulated by carbachol and GSNO was inhibited by addition of the sGC inhibitor, ODQ, and cGMP-dependent protein kinase inhibitor, KT-5823. These results indicate that amylase release may be mediated through the NO/cGMP signaling pathway.
Author Shimomura, Hiromi
Komine, Nobuhiro
Tanaka, Satoshi
Nashida, Tomoko
Shimooka, Shohachi
Imai, Akane
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Keywords Nitrogen oxide
Rat parotid gland
Amylase
YC-1
cGMP
GSNO
ODQ
Guanylyl cyclase
sGC
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Snippet It is well known that the muscarinic cholinergic agonists, carbachol and methacholine, enhance nitric oxide synthase (NOS) activity, and also stimulate...
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SubjectTerms Amylase
Amylases - analysis
Amylases - secretion
Animals
Carbachol - pharmacology
Cells, Cultured
cGMP
Cyclic GMP - analysis
Cyclic GMP - metabolism
Dentistry
Dose-Response Relationship, Drug
Enzyme Activators - pharmacology
Guanylate Cyclase - analysis
Guanylate Cyclase - antagonists & inhibitors
Guanylyl cyclase
Indazoles - pharmacology
Male
Muscarinic Agonists - pharmacology
Nitric Oxide - metabolism
Nitric Oxide Donors - pharmacology
Nitrogen oxide
Parotid Gland - drug effects
Parotid Gland - enzymology
Parotid Gland - secretion
Rat parotid gland
Rats
Rats, Wistar
S-Nitrosoglutathione - pharmacology
Signal Transduction - physiology
Title Soluble guanylyl cyclase is localised in the acinar cells and participates in amylase secretion in rat parotid gland
URI https://dx.doi.org/10.1016/j.archoralbio.2004.03.001
https://www.ncbi.nlm.nih.gov/pubmed/15275856
https://search.proquest.com/docview/66742415
Volume 49
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