Endothelial nitric oxide modulatory role on vascular sympathetic reactivity

• Type: Other Publications
• Date: 2013

Authors

Sousa, JB (Author) Other; Fresco, P (Author) FFUP; Diniz, C (Author) FFUP

Scientific classification

FOS: Medical and Health sciences > Basic medicine

Other information

Authenticus ID: P-006-FZT

Abstract (EN): Conflicting data suggests that NO may influence noradrenaline release from vascular postgangliconic sympathetic nerves. Some studies indicate that NO promote an inhibition while others indicate the involvement of NO in the facilitation of noradrenaline release. We aim at investigating the role of NO in vascular sympathetic neurotransmission in the mesenteric and tail arteries. The influence of NO on noradrenaline release was found to be distinct between mesenteric and tail arteries with a pronounced enhancement of noradrenaline release caused by NO mediated activation in intact tail arteries: DEA NONOate (10 mu M), a NO donor, facilitated tritium overflow up to 18,80 +/- 0.10% or by the inhibition (up to -25,79 +/- 0,045% obtained in the presence of L-NAME (100 mu M), a NO synthase inhibitor. In denuded arteries L-Name (100 mu M) failed to modify noradrenaline release. DEA NONOate (10 mu M) and SNP (100 mu M), two different NO donors caused an inhibition in noradrenaline release in denuded arteries, -18,92 +/- 0,15% and -24,42 +/- 0,061%, respectively. Data indicate that the signalling pathway activated by exogenous NO, ultimately causes a reduction in noradrenaline release in denuded tail arteries, in opposition to the effects observed in intact tail arteries. Endogenous NO, produced most probably in the endothelium, in turn, mediate an enhancement of noradrenaline release. These indicate that NO from different sources can induce opposite effects probably through activation/ influence of distinct pathways.

Language: English

Type (Professor's evaluation): Scientific