Ecto‐AMP Deaminase Blunts the ATP‐Derived Adenosine A<sub>2A</sub> Receptor Facilitation of Acetylcholine Release at Rat Motor Nerve Endings

Magalhães-Cardoso, M.T.; Pereira, M. Fátima; Oliveira, Luis; Ribeiro, J.A.; Cunha, Rodrigo A.; Correia‐de‐Sá, P.

doi:10.1113/jphysiol.2003.040410

Cited by 52 publications

(72 citation statements)

References 41 publications

(81 reference statements)

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“…Samples (75 l) were collected from each well at different times up to 30 min for high performance liquid chromatography (HPLC) (LaChrome Elite, Merck) analysis of the variation of substrate disappearance and product formation (11,20). ATP and ADP catabolism analysis was performed by ion pair reverse-phase HPLC (21), whereas AMP catabolism analysis used a linear gradient (100% 100 mM KH 2 PO 4 , pH 7, to 100% 100 mM KH 2 PO 4 , pH 7, 30% methanol) for 10 min with a constant rate flow of 1.25 ml/min.…”

Section: Methodsmentioning

confidence: 99%

Histamine Induces ATP Release from Human Subcutaneous Fibroblasts, via Pannexin-1 Hemichannels, Leading to Ca2+ Mobilization and Cell Proliferation

Pinheiro

Paramos-de-Carvalho²,

Certal³

et al. 2013

Journal of Biological Chemistry

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Changes in the regulation of connective tissue ATP-mediated mechano-transduction and remodeling may be an important link to the pathogenesis of chronic pain. It has been demonstrated that mast cell-derived histamine plays an important role in painful fibrotic diseases. Here we analyzed the involvement of ATP in the response of human subcutaneous fibroblasts to histamine. Acute histamine application caused a rise in intracellular Ca2+ ([Ca2+]i) and ATP release from human subcutaneous fibroblasts via H1 receptor activation. Histamine-induced [Ca2+]i rise was partially attenuated by apyrase, an enzyme that inactivates extracellular ATP, and by blocking P2 purinoceptors with pyridoxal phosphate-6-azo(benzene-2,4-disulfonic acid) tetrasodium salt and reactive blue 2. [Ca2+]i accumulation caused by histamine was also reduced upon blocking pannexin-1 hemichannels with 10Panx, probenecid, or carbenoxolone but not when connexin hemichannels were inhibited with mefloquine or 2-octanol. Brefeldin A, an inhibitor of vesicular exocytosis, also did not block histamine-induced [Ca2+]i mobilization. Prolonged exposure of human subcutaneous fibroblast cultures to histamine favored cell growth and type I collagen synthesis via the activation of H1 receptor. This effect was mimicked by ATP and its metabolite, ADP, whereas the selective P2Y1 receptor antagonist, MRS2179, partially attenuated histamine-induced cell growth and type I collagen production. Expression of pannexin-1 and ADP-sensitive P2Y1 receptor on human subcutaneous fibroblasts was confirmed by immunofluorescence confocal microscopy and Western blot analysis. In conclusion, histamine induces ATP release from human subcutaneous fibroblasts, via pannexin-1 hemichannels, leading to [Ca2+]i mobilization and cell growth through the cooperation of H1 and P2 (probably P2Y1) receptors.

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Section: Methodsmentioning

confidence: 99%

Histamine Induces ATP Release from Human Subcutaneous Fibroblasts, via Pannexin-1 Hemichannels, Leading to Ca2+ Mobilization and Cell Proliferation

Pinheiro

Paramos-de-Carvalho²,

Certal³

et al. 2013

Journal of Biological Chemistry

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“…In fact, several studies have shown that stimulated nerve terminals can directly release ATP, which is stored in synaptic vesicles (reviewed in Sperlágh and Vizi, 1996). However, this stimulation-evoked release of ATP from nerve terminals seems to differ from the release of classical neurotransmitters (Farinas et al, 1992;Magalhães-Cardoso et al, 2003;Rabasseda et al, 1987;Santos et al, 1999; see also Coco et al, 2003). In particular, this release of ATP is disproportionally larger at higher frequencies of nerve stimulation (Cunha et al, 1996a;Wieraszko et al, 1989).…”

Section: Adenosine As a Synaptic Modulator-a 2a Receptorsmentioning

confidence: 99%

Different cellular sources and different roles of adenosine: A1 receptor-mediated inhibition through astrocytic-driven volume transmission and synapse-restricted A2A receptor-mediated facilitation of plasticity

Cunha

2008

Neurochemistry International

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146

129

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Adenosine is a prototypical neuromodulator, which mainly controls excitatory transmission through the activation of widespread inhibitory A 1 receptors and synaptically located A 2A receptors. It was long thought that the predominant A 1 receptor-meditated modulation by endogenous adenosine was a homeostatic process intrinsic to the synapse. New studies indicate that endogenous extracellular adenosine is originated as a consequence of the release of gliotransmitters, namely ATP, which sets a global inhibitory tonus in brain circuits rather than in a single synapse. Thus, this neuron-glia long-range communication can be viewed as a form of non-synaptic transmission (a concept introduced by Professor Sylvester Vizi), designed to reduce noise in a circuit. This neuron-glia-induced adenosine release is also responsible for exacerbating salient information through A 1 receptor-mediated heterosynaptic depression, whereby the activation of a particular synapse recruits a neuron-glia network to generate extracellular adenosine that inhibits neighbouring non-tetanised synapses. In parallel, the local activation of facilitatory A 2A receptors by adenosine, formed from ATP released only at high frequencies from neuronal vesicles, down-regulates A 1 receptors and facilitates plasticity selectively in the tetanised synapse. Thus, upon high-frequency firing of a given pathway, the combined exacerbation of global A 1 receptormediated inhibition in the circuit (heterosynaptic depression) with the local synaptic activation of A 2A receptors in the activated synapse, cooperate to maximise salience between the activated and non-tetanised synapses. #

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“…After a 30-min equilibration period, the preparations were incubated with 30 M adenosine (zero time). Samples of 75 l were collected from the organ bath at different times up to 45 min for high-performance liquid chromatography (L-6200 Intelligent pump with an L-4000 UV detector; Hitachi, Sachen, Germany) analysis of the variation of substrate disappearance and product formation (Magalhã es-Cardoso et al, 2003). Concentrations of the substrate and products were plotted as a function of time (progress curves).…”

Section: Methodsmentioning

confidence: 99%

Corpus Cavernosum from Men with Vasculogenic Impotence Is Partially Resistant to Adenosine Relaxation due to Endothelial A_2BReceptor Dysfunction

Faria

Magalhães-Cardoso²,

Lafuente-de-Carvalho³

et al. 2006

J Pharmacol Exp Ther

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Although adenosine has been implicated in penile erection in human males, the receptor subtype responsible for adenosine regulation of human corpus cavernosum (HCC) smooth muscle tone is still a matter of debate. Using selective adenosine agonists and antagonists, we aimed at characterizing the adenosine receptors mediating relaxation of precontracted (with 1 M phenylephrine) HCC strips. HCC specimens were collected from control subjects (organ donors) and from patients with severe vasculogenic erectile dysfunction (ED). In control subjects, adenosine and 5Ј-N-ethyl-carboxamide adenosine (NECA) fully relaxed HCC. The selective A 2A receptor agonist 2-[4-(2-p-carboxy ethyl)phenylamino]-5Ј-N-ethylcarboxamido adenosine (CGS21680C) produced only a partial relaxation (30 -50%) of HCC, which could be further enhanced by simultaneous application of 100 M NECA. The selective A 2B receptor antagonist N-(4-acetylphenyl)-2- [4-(2,3,6,7-tetrahydro-2,6-dioxo-1,3-dipropyl-1H-purin-8-il) (ZM241385) (50 nM) consistently reduced the actions of both agonists. In contrast to CGS21680C, NECAinduced relaxation was attenuated when endothelial production of NO and prostanoids was reduced by 100 M N G -nitro-Larginine and 10 M indomethacin, respectively. HCC strips from patients with vasculogenic ED were partially resistant to NECA but kept relaxation to CGS21680C; the remaining effect was sensitive to blockade of A 2A receptors with 50 nM ZM241385. Data suggest that adenosine regulates HCC smooth muscle tone through the activation of two receptor populations, CGS21680C-sensitive (A 2A ) and -insensitive (A 2B ) receptors, located on smooth muscle fibers and on endothelial cells, respectively. Endothelial dysfunction may be correlated with a loss of adenosine A 2B receptor activity in penile vessels from men with vasculogenic ED.

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Ecto‐AMP Deaminase Blunts the ATP‐Derived Adenosine A_2A Receptor Facilitation of Acetylcholine Release at Rat Motor Nerve Endings

Cited by 52 publications

References 41 publications

Histamine Induces ATP Release from Human Subcutaneous Fibroblasts, via Pannexin-1 Hemichannels, Leading to Ca2+ Mobilization and Cell Proliferation

Histamine Induces ATP Release from Human Subcutaneous Fibroblasts, via Pannexin-1 Hemichannels, Leading to Ca2+ Mobilization and Cell Proliferation

Different cellular sources and different roles of adenosine: A1 receptor-mediated inhibition through astrocytic-driven volume transmission and synapse-restricted A2A receptor-mediated facilitation of plasticity

Corpus Cavernosum from Men with Vasculogenic Impotence Is Partially Resistant to Adenosine Relaxation due to Endothelial A_2BReceptor Dysfunction

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Ecto‐AMP Deaminase Blunts the ATP‐Derived Adenosine A2A Receptor Facilitation of Acetylcholine Release at Rat Motor Nerve Endings

Cited by 52 publications

References 41 publications

Histamine Induces ATP Release from Human Subcutaneous Fibroblasts, via Pannexin-1 Hemichannels, Leading to Ca2+ Mobilization and Cell Proliferation

Histamine Induces ATP Release from Human Subcutaneous Fibroblasts, via Pannexin-1 Hemichannels, Leading to Ca2+ Mobilization and Cell Proliferation

Different cellular sources and different roles of adenosine: A1 receptor-mediated inhibition through astrocytic-driven volume transmission and synapse-restricted A2A receptor-mediated facilitation of plasticity

Corpus Cavernosum from Men with Vasculogenic Impotence Is Partially Resistant to Adenosine Relaxation due to Endothelial A2BReceptor Dysfunction

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Ecto‐AMP Deaminase Blunts the ATP‐Derived Adenosine A_2A Receptor Facilitation of Acetylcholine Release at Rat Motor Nerve Endings

Corpus Cavernosum from Men with Vasculogenic Impotence Is Partially Resistant to Adenosine Relaxation due to Endothelial A_2BReceptor Dysfunction