Differential inhibition of noradrenaline release mediated by inhibitory A1-adenosine receptors in the mesenteric vein and artery from normotensive and hypertensive rats

Rocha-Pereira, Carolina; Sousa, Joana Beatriz; Vieira-Rocha, Maria Sofia; Fresco, Paula; Gonçalves, Jorge; Diniz, Carmen

doi:10.1016/j.neuint.2013.02.010

Cited by 9 publications

(14 citation statements)

References 32 publications

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“…[ 3 H]-noradrenaline release experiments were carried out as previously described [23,24,27–29]. Briefly, the arterial segments were pre-incubated in 2 ml Krebs-Henseleit solution containing 0.1 μmol/L [ 3 H]- noradrenaline (for 60 min at 37°C) and transferred to superfusion chambers, superfused with [ 3 H]-noradrenaline-free medium (1 ml.min-1; constant rate: Krebs-Henseleit solution with desipramine 400 nmol/L to inhibit noradrenaline’s neuronal uptake).…”

Section: Methodsmentioning

confidence: 99%

“…At the end of the experiments (t = 130 min), tritium was measured in superfusate samples and solubilized arteries (sonicated for 1h with 2.5 ml perchloric acid (0.2 mol/L)) by liquid scintillation spectrometry (LS 6500, Beckman Instruments, Fullerton, USA) after adding 6 ml of a scintillation mixture (OptiPhase ‘Hisafe’ 3, PerkinElmer, I.L.C., Lisboa, Portugal) to each sample. Tissue labelling with [ 3 H]-noradrenaline and evaluation of electrically-evoked tritium overflow changes was performed as previously described [23,24]. …”

Section: Methodsmentioning

confidence: 99%

“…Therefore, it is possible that adenosine and its receptors (adenosine receptors) might participate on the modulation of sympathetic neurotransmission exerted by NO. It is worth noting that we have previously demonstrated that adenosine receptors are present in perivascular sympathetic nerves modulating noradrenaline release in mesenteric [23–25] and tail arteries [26–30]. …”

Section: Introductionmentioning

confidence: 99%

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Endothelial and Neuronal Nitric Oxide Activate Distinct Pathways on Sympathetic Neurotransmission in Rat Tail and Mesenteric Arteries

et al. 2015

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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.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Endothelial and Neuronal Nitric Oxide Activate Distinct Pathways on Sympathetic Neurotransmission in Rat Tail and Mesenteric Arteries

et al. 2015

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“…Tissue labelling with [ 3 H]-noradrenaline and the evaluation of electrically-evoked tritium overflow changes were performed as previously described [12], [13]. Effects of agonists (CPA, CGS 21680), of antagonists (DPCPX, SCH 58261), and of enzyme (pentostatin, ITU, α,β-methylene ADP) and nucleoside transport (NBTI) inhibitors were studied.…”

Section: Methodsmentioning

confidence: 99%

“…In vessels, the involvement of adenosine receptors in sympathetic modulation has been described both in arteries[6]–[13] and in veins [12]. A reduced effect mediated by selective adenosine A 1 , but not A 2A receptor agonists in sympathetic vascular neurotransmission in hypertensive state has been reported [13].…”

Section: Introductionmentioning

confidence: 98%

Lack of Endogenous Adenosine Tonus on Sympathetic Neurotransmission in Spontaneously Hypertensive Rat Mesenteric Artery

et al. 2014

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BackgroundIncreased sympathetic activity has been implicated in hypertension. Adenosine has been shown to play a role in blood flow regulation. In the present study, the endogenous adenosine neuromodulatory role, in mesenteric arteries from normotensive and spontaneously hypertensive rats, was investigated.Methods and ResultsThe role of endogenous adenosine in sympathetic neurotransmission was studied using electrically-evoked [3H]-noradrenaline release experiments. Purine content was determined by HPLC with fluorescence detection. Localization of adenosine A1 or A2A receptors in adventitia of mesenteric arteries was investigated by Laser Scanning Confocal Microscopy. Results indicate a higher electrically-evoked noradrenaline release from hypertensive mesenteric arteries. The tonic inhibitory modulation of noradrenaline release is mediated by adenosine A1 receptors and is lacking in arteries from hypertensive animals, despite their purine levels being higher comparatively to those determined in normotensive ones. Tonic facilitatory adenosine A2A receptor-mediated effects were absent in arteries from both strains. Immunohistochemistry revealed an adenosine A1 receptors redistribution from sympathetic fibers to Schwann cells, in adventitia of hypertensive mesenteric arteries which can explain, at least in part, the absence of effects observed for these receptors.ConclusionData highlight the role of purines in hypertension revealing that an increase in sympathetic activity in hypertensive arteries is occurring due to a higher noradrenaline/ATP release from sympathetic nerves and the loss of endogenous adenosine inhibitory tonus. The observed nerve-to-glial redistribution of inhibitory adenosine A1 receptors in hypertensive arteries may explain the latter effect.

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Vascular impairment of adenosinergic system in hypertension: increased adenosine bioavailability and differential distribution of adenosine receptors and nucleoside transporters

Sousa-Oliveira

Brandão

Vojtek

et al. 2018

Histochem Cell Biol

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Differential inhibition of noradrenaline release mediated by inhibitory A1-adenosine receptors in the mesenteric vein and artery from normotensive and hypertensive rats

Cited by 9 publications

References 32 publications

Endothelial and Neuronal Nitric Oxide Activate Distinct Pathways on Sympathetic Neurotransmission in Rat Tail and Mesenteric Arteries

Endothelial and Neuronal Nitric Oxide Activate Distinct Pathways on Sympathetic Neurotransmission in Rat Tail and Mesenteric Arteries

Lack of Endogenous Adenosine Tonus on Sympathetic Neurotransmission in Spontaneously Hypertensive Rat Mesenteric Artery

Vascular impairment of adenosinergic system in hypertension: increased adenosine bioavailability and differential distribution of adenosine receptors and nucleoside transporters

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