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.
Highlights
Nitric oxide (NO) contributes to vascular homeostasis [1,2,3] by modulating the vascular dilator tone and regulating local cell growth
Inhibition of electrically-evoked tritium overflow induced by DEA/ NONOate was abolished by the selective adenosine A1 receptors antagonist, DPCPX (20 nM), Table 1
Laser scanning confocal microscopy (LSCM) images from the adventitial layers, of both mesenteric and tail arteries, exhibited nNOS isoform immunoreactivities (Fig 4A), but quantitative analysis evidenced that the relative amount of nNOS immunoreactivity present in tail arteries is lower than that exhibited in mesenteric arteries (Fig 4B)
Summary
Nitric oxide (NO) contributes to vascular homeostasis [1,2,3] by modulating the vascular dilator tone and regulating local cell growth. There are conflicting data concerning the influence exerted by NO on noradrenaline release: some authors claim that NO inhibits [17,18] whereas other studies showed an increase in noradrenaline release caused by NO [19,20,21]. Most of these studies have been performed in heart, brain or urethra and, information on the direct influence of NO on perivascular sympathetic transmission is not fully understood
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