Endothelial nitric oxide modulatory role on vascular sympathetic reactivity

摘要

Conflicting data suggests that NO may influence noradrenaline release from vascular postgangliconicsympathetic nerves. Some studies indicate that NO promote an inhibition while others indicate the involvementof NO in the facilitation of noradrenaline release. We aim at investigating the role of NO in vascular sympatheticneurotransmission in the mesenteric and tail arteries. The influence of NO on noradrenaline release was found tobe distinct between mesenteric and tail arteries with a pronounced enhancement of noradrenaline release causedby NO mediated activation in intact tail arteries: DEA NONOate (10 μM), a NO donor, facilitated tritiumoverflow up to 18,80±0.10% or by the inhibition (up to -25,79±0,045% obtained in the presence of L-NAME(100 μM), a NO synthase inhibitor. In denuded arteries L-Name (100 μM) failed to modify noradrenalinerelease. DEA NONOate (10 μM) and SNP (100 μM), two different NO donors caused an inhibition innoradrenaline release in denuded arteries, -18,92±0,15% and -24,42±0,061%, respectively. Data indicate that thesignalling pathway activated by exogenous NO, ultimately causes a reduction in noradrenaline release indenuded tail arteries, in opposition to the effects observed in intact tail arteries. Endogenous NO, produced mostprobably in the endothelium, in turn, mediate an enhancement of noradrenaline release. These indicate that NOfrom different sources can induce opposite effects probably through activation/ influence of distinct pathways.Keywords: Endothelium, nitric oxide, vascular sympathetic nerves, noradrenaline.