Hydrogen sulfide: a novel gaseous signaling molecule and intracellular [Ca.sup.2+] regulator in rat parotid acinar cells

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Date: Oct. 2015
Publisher: American Physiological Society
Document Type: Author abstract; Report
Length: 221 words

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Abstract :

In addition to nitric oxide (NO), hydrogen sulfide ([H.sub.2]S) is recognized as a crucial gaseous messenger that exerts many biological actions in various tissues. An attempt was made to assess the roles and underlying mechanisms of both gases in isolated rat parotid acinar cells. Ductal cells and some acinar cells were found to express NO and [H.sub.2]S synthases. Cevimeline, a muscarinic receptor agonist upregulated endothelial NO synthase in parotid tissue. NO and [H.sub.2]S donors increased the intracellular [Ca.sup.2+] concentration ([[[Ca.sup.2+]].sub.i]). This was not affected by inhibitors of phospholipase C and inositol 1,4,5-trisphosphate receptors, but was decreased by blockers of ryanodine receptors (RyRs), soluble guanylyl cyclase, and protein kinase G. The [H.sub.2]S donor evoked NO production, which was decreased by blockade of NO synthases or phosphoinositide 3-kinase or by hypotaurine, an [H.sub.2]S scavenger. The [H.sub.2]S donor-induced [[[Ca.sup.2+]].sub.i] increase was diminished by a NO scavenger or the NO synthases blocker. These results suggest that NO and [H.sub.2]S play important roles in regulating [[[Ca.sup.2+]].sub.i] via soluble guanylyl cyclase-cGMP-protein kinase G-RyRs, but not via inositol 1,4,5-trisphosphate receptors. The effect of [H.sub.2]S may be partially through NO produced via phosphoinositide 3-kinase-Akt-endothelial NO synthase. It was concluded that both gases regulate [[[Ca.sup.2+]].sub.i] in a synergistic way, mainly via RyRs in rat parotid acinar cells. hydrogen sulfide; intracellular [Ca.sup.2+]; ryanodine receptors; nitric oxide; parotid acinar cells doi: 10.1152/ajpcell.00147.2015

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Gale Document Number: GALE|A435356893