| Impairment of acetylcholine-mediated endothelium-dependent relaxation in isolated parotid artery of the alloxan-induced diabetic rabbit. | |
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MedLine Citation:
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PMID: 21896051 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Roganović J, Radenković M, Tanić N, Tanić N, Petrović N, Stojić D. Impairment of acetylcholine-mediated endothelium-dependent relaxation in isolated parotid artery of the alloxan-induced diabetic rabbit. Eur J Oral Sci 2011; 119: 352-360. © 2011 Eur J Oral Sci The aim of this study was to assess the effect of type 1 diabetes mellitus (induced by a single intravenous injection of 100 mg kg(-1) of alloxan) on acetylcholine (ACh)-induced relaxation in isolated rabbit parotid gland feeding artery. Isometric force measurements and quantification of inducible nitric oxide synthase (iNOS) mRNA by real-time RT-PCR were made in parotid artery rings from diabetic and control rabbits. Acetylcholine induced concentration- and endothelium-dependent vasorelaxation that was significantly decreased in parotid artery rings from diabetic rabbits. Schild analysis of the ACh vasorelaxant effect, in the presence of selective muscarinic receptor antagonists, revealed involvement of the M(3) receptor subtype in parotid artery rings from both control and diabetic rabbits, with no change in antagonist affinity constants. The inhibitory effects of indomethacin, a non-selective inhibitor of cyclooxygenase, and of high potassium, an inhibitor of hyperpolarization, on ACh vasorelaxation were increased. The effect of N(G) -nitro-l-arginine, a non-selective inhibitor of NOS, was decreased in diabetes. S-methylisothiourea, a selective inhibitor of iNOS, significantly reduced ACh vasorelaxation only in parotid artery rings from diabetic rabbits. Also, up-regulation of iNOS mRNA expression was detected in parotid artery rings from diabetic rabbits. These results suggest that in parotid artery rings from diabetic rabbits, impaired endothelium-dependent vasorelaxation to ACh appears to be caused by the loss of a nitric oxide-mediated component and increased iNOS expression, and is unlikely to be caused by a change at the M(3) receptor level. |
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Authors:
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Jelena Roganović; Miroslav Radenković; Nikola Tanić; Nasta Tanić; Nina Petrović; Dragica Stojić |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: European journal of oral sciences Volume: 119 ISSN: 1600-0722 ISO Abbreviation: Eur. J. Oral Sci. Publication Date: 2011 Oct |
Date Detail:
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Created Date: 2011-09-07 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9504563 Medline TA: Eur J Oral Sci Country: Denmark |
Other Details:
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Languages: eng Pagination: 352-60 Citation Subset: D; IM |
Copyright Information:
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© 2011 Eur J Oral Sci. |
Affiliation:
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Department of Pharmacology, Faculty of Dentistry, University of Belgrade, Belgrade Department of Clinical Pharmacology, Pharmacology and Toxicology, Medical Faculty, University of Belgrade, Belgrade Department of Neurobiology, Institute for Biological Research 'Siniša Stanković', University of Belgrade, Belgrade Department of Radiobiology and Molecular Genetics, Institute of Nuclear Sciences 'Vinča', Belgrade, Serbia. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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