Endothelial and neuronal nitric oxide activate distinct pathways on sympathetic neurotransmission in rat tail and mesenteric arteries
Entity
UAM. Departamento de FisiologíaPublisher
Public Library of ScienceDate
2015-06-15Citation
10.1371/journal.pone.0129224
PLos ONE 10.6 (2015): e0129224
ISSN
1932-6203DOI
10.1371/journal.pone.0129224Funded by
This work was supported by FEDER through Program of Operational Competitiveness Factors - COMPETE and by National Funds through Foundation for Science and Technology (FCT): Grant N°. PEst C/EQB/LA0006/2011. JBS was supported by PhD grant (SFRH/BD//2009) - FCT (URL: http:// www.fct.pt/)Editor's Version
http://dx.doi.org/10.1371/journal.pone.0129224Subjects
Neurotransmission; Neuronal; Arteries; MedicinaRights
© 2015 Sousa et al.Abstract
Nitric oxide (NO) seems to contribute to vascular homeostasis regulating neurotransmission.
This work aimed at assessing the influence of NO from different sources and respective
intracellular pathways on sympathetic neurotransmission, in two vascular beds.
Electrically-evoked [3H]-noradrenaline release was assessed in rat mesenteric and tail arteries
in the presence of NO donors or endothelial/neuronal nitric oxide synthase (NOS)
inhibitors. The influence of NO on adenosine-mediated effects was also studied using selective
antagonists for adenosine receptors subtypes. Location of neuronal NOS (nNOS)
was investigated by immunohistochemistry (with specific antibodies for nNOS and for
Schwann cells) and Confocal Microscopy. Results indicated that: 1) in mesenteric arteries,
noradrenaline release was reduced by NO donors and it was increased by nNOS inhibitors;
the effect of NO donors was only abolished by the adenosine A1 receptors antagonist; 2)
in tail arteries, noradrenaline release was increased by NO donors and it was reduced by
eNOS inhibitors; adenosine receptors antagonists were devoid of effect; 3) confocal microscopy
showed nNOS staining in adventitial cells, some co-localized with Schwann cells.
nNOS staining and its co-localization with Schwann cells were significantly lower in tail compared
to mesenteric arteries. In conclusion, in mesenteric arteries, nNOS, mainly located in
Schwann cells, seems to be the main source of NO influencing perivascular sympathetic
neurotransmission with an inhibitory effect, mediated by adenosine A1 receptors activation.
Instead, in tail arteries endothelial NO seems to play a more relevant role and has a facilitatory
effect, independent of adenosine receptors activation
Files in this item
Google Scholar:Sousa, Joana Beatriz
-
Vieira-Rocha, Maria Sofia
-
Arribas Rodríguez, Silvia Magdalena
-
González, Maria Carmen
-
Fresco, Paula
-
Diniz, Carmen
This item appears in the following Collection(s)
Related items
Showing items related by title, author, creator and subject.