| Autor: |
Anderson, Leigh C., Martinx, David J., Phillips, Dallen L., Killpack, Kenneth J., Bone, Sven E., Rahimian, Roshanak |
| Předmět: |
|
| Zdroj: |
Experimental Physiology; Mar2006, Vol. 91 Issue 2, p435-444, 10p, 1 Chart, 6 Graphs |
| Abstrakt: |
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 Nω-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 ofl-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 ofl-NAME and indomethacin were dependent on the order of administration and on gender. Followingl-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 byl-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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
Plný text