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This Article Full Text Full Text (PDF) All Versions of this Article: 91/2/435    most recent expphysiol.2005.032730v1 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 Anderson, L. C. Articles by Rahimian, R. Search for Related Content PubMed PubMed Citation Articles by Anderson, L. C. Articles by Rahimian, R.

¹ Department of Anatomical Sciences² Dental Program, Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, CA 94115, USA³ Department of Physiology and Pharmacology, T. J. Long School of Pharmacy and Health Sciences, University of the Pacific, Stockton, CA 95211, USA

Parasympathetic vasodilatation in the rat submandibular gland is mediated by nitric oxide-dependent and -independent mechanisms (prostacyclin and endothelium-derived hyperpolarizing factor (EDHF)). The purpose of this study was to determine the influence of gender on the relative contributions of each pathway to nerve-stimulated vasodilatation. Absolute increases in perfusion (laser Doppler flowmetry) were similar in male and female rats (in arbitrary perfusion units: 6159 ± 4530 and 5601 ± 3877 at 2 Hz; 15645 ± 6830 and 14848 ± 6118 at 5 Hz; and 22418 ± 7660 and 18878 ± 5864 at 10 Hz). However, expressed as a percentage increase above resting values, stimulated perfusion was higher in males than in females (P < 0.05). In males both N-nitro-L-arginine methyl ester (L-NAME) and indomethacin partly blocked parasympathetic vasodilatation at all frequencies tested (P < 0.05). In female rats significant reductions in nerve-stimulated perfusion were observed only at 2 and 5 Hz, but the effects of L-NAME were greater than in males (–64 compared with –45% at 2 Hz and –45 compared with –33% at 5 Hz, P < 0.05). Indomethacin by itself had no apparent effect in females. The combined effects of L-NAME and indomethacin were dependent on the order of administration and on gender. Following L-NAME, indomethacin had no further effect in males or females. L-NAME reduced indomethacin-resistant vasodilatation in males and females, but the added effect of indomethacin was more pronounced in males. Finally, atropine-resistant vasodilatation was partly blocked by L-NAME, and the remaining vasodilatation was abolished by spantide I (substance P receptor antagonist). We conclude that NO, products of cyclo-oxygenase activity and EDHF all play a role in parasympathetic vasodilatation, but that NO and EDHF are the major endothelium-derived vasodilators in the rat submandibular gland. In addition, when other pathways are blocked EDHF makes a greater contribution in females. Lastly, both vasoactive intestinal peptide and substance P contribute to the atropine-resistant vasodilatation.

(Received 8 November 2005; accepted after revision 9 December 2005; first published online 19 December 2005)
Corresponding author L. C. Anderson: Department of Anatomical Sciences, University of the Pacific, Arthur A. Dugoni School of Dentistry, San Francisco, CA 94115, USA. Email: landerso{at}pacific.edu