The influence of gender on parasympathetic vasodilatation in the submandibular gland of the rat.
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 Nomega-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.
Anderson
Leigh C
LC
Department of Anatomical Sciences, University of the Pacific, San Francisco, CA 94115, USA. landerso@pacific.edu
Martin
David J
DJ
Phillips
Dallen L
DL
Killpack
Kenneth J
KJ
Bone
Sven E
SE
Rahimian
Roshanak
R
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001685:Biological Factors / Q000378:metabolism; D001808:Blood Vessels / Q000187:drug effects / Q000294:innervation* / Q000378:metabolism; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004558:Electric Stimulation; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010275:Parasympathetic Nervous System / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012737:Sex Factors; D013363:Submandibular Gland / Q000098:blood supply*; D014664:Vasodilation
D001685:Biological Factors; D016861:Cyclooxygenase Inhibitors; D018727:Muscarinic Antagonists; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide; D001285:Atropine; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin