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This Article Full Text Full Text (PDF) All Versions of this Article: 91/6/977    most recent expphysiol.2006.034710v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Çevik Aras, H. Articles by Ekström, J. Search for Related Content PubMed PubMed Citation Articles by Çevik Aras, H. Articles by Ekström, J. Related Collections GI & Epithelial

Department of ¹ Pharmacology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at Göteborg University, Medicinaregatan 15 D, 405 30 Göteborg, Sweden

Infusion of pentagastrin (20 µg kg^–1 h^–1, I.V.) for 10 min evokes protein output but no overt fluid secretion from the parotid gland of the rat, as revealed by increased protein concentration in a subsequent wash-out flow of saliva in response to a bolus injection of methacholine (5 µg kg^–1, I.V.) 10 min later. Using this experimental set-up, the contribution of nitric oxide (NO) generation to the protein and amylase response evoked by pentagastrin was investigated. Neither the neuronal type NO synthase inhibitor N-propyl-L-arginine (N-PLA; 30 mg kg^–1, I.V.) nor the non-selective NO synthase inhibitor L-NAME (30 mg kg^–1, I.V.) as such affected the methacholine-evoked volume response or the outputs of protein and amylase. However, when preceeded by the pentagastrin infusion, the expected increases in concentrations of protein (145%) and amylase activity (127%) of the methacholine-evoked response (compared to a pre-infusion methacholine response) were reduced to 68 and 74%, respectively, in the presence of N-PLA, and to 70 and 63%, respectively, in the presence of L-NAME. Thus, NO generation resulting from the activity of the neuronal type NO synthase, most probably of parenchymal origin, plays an important role in the pentagastrin-induced protein and amylase secretion of the rat parotid gland.

(Received 13 June 2006; accepted after revision 21 July 2006; first published online 17 July 2006)
Corresponding author J. Ekström: Department of Pharmacology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at Göteborg University, Medicinaregatan 15 D, 405 30 Göteborg, Sweden. Email: jorgen.ekstrom{at}pharm.gu.se