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This Article Full Text Full Text (PDF) All Versions of this Article: 91/4/673    most recent expphysiol.2006.033639v1 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 HighWire Citing Articles via Google Scholar Google Scholar Articles by Aras, H. C. Articles by Ekström, J. Search for Related Content PubMed PubMed Citation Articles by Aras, H. C. Articles by Ekström, J. Related Collections GI & Epithelial

¹ Department of Pharmacology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at Göteborg University, Medicinaregatan 15 D, Box 431, 405 30 Göteborg, Sweden

In parotid glands of pentobarbitone-anaesthetized rats, the incorporation of [³H]leucine into trichloroacetic acid-insoluble materials, reflecting protein synthesis, increased by 17% (compared to saline-treated rats) in response to infusion of pentagastrin (20 µg kg^–1, I.V. for 1 h) under muscarinic and - and ß-adrenoceptor blockade. Both the CCK-A receptor antagonist lorglumide (48 mg kg^–1, I.V.) and the CCK-B receptor antagonist itriglumide (5.5 mg kg^–1, I.V.), given separately, prevented the expected increase in pentagastrin and, in addition, reduced the glandular protein synthesis by 16 and 12%, respectively, below the level of saline-treated rats. In rats treated with saline only, the glandular protein synthesis was reduced by 22% by the CCK-A receptor antagonist and by 17% by the CCK-B receptor antagonist; combined, the two antagonists caused no further reduction (20%). There was no increase in the glandular protein synthesis of pentagastrin-treated rats compared to that of the saline-treated rats when both groups of rats were exposed to a combination of the two types of CCK receptor antagonists. In pentagastrin-treated rats, the protein synthesis in the parotid glands was 23% less in the presence of the non-selective nitric oxide (NO) synthase inhibitor L-NAME (30 mg kg^–1, I.V.) than in its absence; the result was the same (23%) when the neuronal NO synthase inhibitor N-propyl-L-arginine (N-PLA; 30 mg kg^–1, I.V.) replaced L-NAME. The protein synthesis in rats treated with saline only was not reduced by L-NAME; nor was the protein synthesis of saline-treated rats different from that of pentagastrin- and L-NAME-treated rats. Thus, under ‘basal’ conditions, a portion of the glandular protein synthesis, as well as the whole increase in synthesis in response to administration of pentagastrin, engaged both types of CCK receptors. Furthermore, NO generation, owing to neuronal NO synthase activity, was required for the increase to occur in response to pentagastrin, whereas a non-NO-dependent pathway was responsible for the protein synthesis under ‘basal’ conditions.

(Received 16 February 2006; accepted after revision 23 March 2006; first published online 23 March 2006)
Corresponding author J. Ekström: Department of Pharmacology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at Göteborg University, Medicinaregatan 15 D, Box 431, 405 30 Göteborg, Sweden. Email: jorgen.ekstrom{at}pharm.gu.se

This article has been cited by other articles:

				H. Cevik Aras and J. Ekstrom Pentagastrin-induced nitric oxide-dependent protein secretion from the parotid gland of the anaesthetized rat Exp Physiol, November 1, 2006; 91(6): 977 - 982. [Abstract] [Full Text] [PDF]