Mediators of Inflammation

Mediators of Inflammation / 2002 / Article

Open Access

Volume 11 |Article ID 698427 | https://doi.org/10.1080/0962935021000051520

Enri Borda, Graciela Stranieri, Leonor Sterin-Borda, "H1-Receptor activation triggers the endogenous nitric oxide signalling system in the rat submandibular gland", Mediators of Inflammation, vol. 11, Article ID 698427, 7 pages, 2002. https://doi.org/10.1080/0962935021000051520

H1-Receptor activation triggers the endogenous nitric oxide signalling system in the rat submandibular gland

Abstract

Background: Histamine is released from mast cells by immunologic and non-immunologic stimuli during salivary gland inflammation, regulating salivary secretion. The receptor-secretory mechanism has not been studied in detail.Aims: The studies reported were directed toward elucidating signal transduction/second messenger pathways within the rat submandibular gland associated with 2-thiazolylethylamine (ThEA)-induced H1-receptor responses.Materials and methods: To assess the H1 receptor subtype expression in the rat submandibular gland, a radioligand binding assay was performed. The study also included inositolphosphates and cyclic GMP accumulation, protein kinase C and nitric oxide synthase activities, and amylase release.Results: The histamine H1 receptor subtype is expressed on the rat submandibular gland with high-affinity binding sites. The ThEA effect was associated with activation of phosphoinositide-specific phospholipase C, translocation of protein kinase C, stimulation of nitric oxide synthase activity and increased production of cyclic GMP. ThEA stimulation of nitric oxide synthase and cyclic GMP was blunted by agents able to interfere with calcium movilization, while a protein kinase C inhibitor was able to stimulate ThEA action. On the other hand, ThEA stimulation evoked amylase release via the H1 receptor but was not followed by the L-arginine/nitric oxide pathway activation.Conclusions: These results suggest that, apart from the effect of ThEA on amylase release, it also appears to be a vasoactive chemical mediator that triggers vasodilatation, modulating the course of inflammation.

Copyright © 2002 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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