The influence of gender on parasympathetic vasodilatation in the submandibular gland of the rat

Authors

Leigh C. Anderson, University of the Pacific
David J. Martin, University of the Pacific
Dallen L. Phillips, University of the Pacific
Kenneth J. Killpack, University of the Pacific
Sven E. Bone, University of the Pacific
Roshanak Rahimian, University of the PacificFollow

Document Type

Article

Publication Title

Experimental Physiology

ISSN

0958-0670

Volume

91

Issue

2

DOI

10.1113/expphysiol.2005.032730

First Page

435

Last Page

444

Publication Date

1-1-2006

Abstract

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. © 2006 The Authors. ω

Recommended Citation

Anderson, L. C., Martin, D. J., Phillips, D. L., Killpack, K. J., Bone, S. E., & Rahimian, R. (2006). The influence of gender on parasympathetic vasodilatation in the submandibular gland of the rat. Experimental Physiology, 91(2), 435–444. DOI: 10.1113/expphysiol.2005.032730
https://scholarlycommons.pacific.edu/phs-facarticles/473