Received November 8, 2005
Revised November 24, 2005
Accepted after revision December 9, 2005
The Influence of Gender on Parasympathetic Vasodilatation in the Submandibular Gland of the Rat
Leigh Anderson 1*,
David Martin 1,
Dallen Phillips 1,
Kenneth Killpack 1,
Sven Bone 1,
Roshanak Rahimian 1
1 University of the Pacific
* To whom correspondence should be addressed. E-mail: landerso{at}pacific.edu.
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Abstract |
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Parasympathetic vasodilatation in the rat submandibular gland is mediated by nitric oxide (NO)-dependent and -independent (prostacyclin and endothelium-derived hyperpolarizing factor [EDHF]) mechanisms. 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 (6159 ± 4530 and 5601 ± 3877 at 2 Hz; 15645 ± 6830 and 14848 ± 6118 at 5 Hz; 22418 ± 7660 and 18878 ± 5864 at 10 Hz). However, expressed as a percent increase above resting values, stimulated perfusion was higher in males than in females (p<0.05). In males, both L-NAME and indomethacin partially blocked parasympathetic vasodilatation at all frequencies tested (p<0.05). In female rats significant reductions in nerve-stimulated perfusion were observed only at 2 Hz 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 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 partially blocked by L-NAME and the remaining vasodilatation was abolished by spantide 1 (substance P receptor antagonist). We conclude that NO, products of cyclooxygenase activity and EDHF all play a role in parasympathetic vasodilatation, but 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 (VIP) and substance P contribute to the atropine-resistant vasodilatation.
Key Words:
Autonomic nervous system, Endothelium, Vasodilatation
