The Hydrolysis of Extracellular Adenine Nucleotides by Arterial Smooth Muscle Cells

Gordon, Ellen L.; Pearson, Jeremy D.; Dickinson, Ellen S.; Moreau, Dimitri; Slakey, Linda L.

doi:10.1016/s0021-9258(19)47255-4

Cited by 91 publications

(7 citation statements)

References 29 publications

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“…The rapid initial rate of catabolism was still observed in these conditions and this lead to an apparent K M value of extracellular catabolism between 400-1200 M, considerably higher than what is found in most systems (reviewed in 40). High K M values of extracellular ATP catabolism were also found in rat ventricular myocytes, in pig arterial smooth muscle cells and in pig aorta endothelial cells and were justified by the hypothesis that the depletion of substrate at the cell surface is rate limiting for hydrolysis of ATP supplied from the bulk phase (41)(42)(43). Interestingly, ecto-ATPase was found to be located in caveolae (44), supporting the possible occurrence of channelling processes.…”

Section: Resultsmentioning

confidence: 83%

“…One issue that can only marginally be addressed with this type of studies is on the molecular entity responsible for the extracellular catabolism of ATP. Some authors favour the view that there are two main different entities, an ecto-ATPase and an ecto-ADPase (24,(41)(42)(43) whereas others champion the idea that the extracellular catabolism of ATP and ADP are mainly due to an ecto-ATP diphosphohydrolase (45)(46)(47). The observed accumulation of ADP upon ATP catabolism (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Cunha

2001

Neurochemical Research

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Ecto-nucleotidases play a pivotal role in terminating the signalling via ATP and in producing adenosine, a neuromodulator in the nervous system. We have now investigated the pattern of adenosine formation with different concentrations of extracellular ATP in rat hippocampal nerve terminals. It was found that adenosine formation is delayed with increasing concentrations of ATP. Also, the rate of adenosine formation increased sharply when the extracellular concentrations of ATP + ADP decrease below 5 microM, indicating that ATP/ADP feed-forwardly inhibit ecto-5'-nucleotidase allowing a burst-like formation of adenosine possibly designed to activate facilitatory A2A receptors. Initial rate measurements of ecto-5'-nucleotidase in hippocampal nerve terminals, using IMP as substrate, showed that ATP and ADP are competitive inhibitors (apparent Ki of 14 and 4 microM). In contrast, in hippocampal immunopurified cholinergic nerve terminals, a burst-like formation of adenosine is not apparent, suggesting that channelling processes may overcome the feed-forward inhibition of ecto-5'-nucleotidase, thus favouring A1 receptor activation.

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Section: Resultsmentioning

confidence: 83%

Section: Resultsmentioning

confidence: 99%

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Cunha

2001

Neurochemical Research

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“…These considerations support the feasibility for the hypothesis that the macula densa cells secrete ATP into the surrounding interstitium where it functions as a paracrine regulator of afferent arteriolar tone (42,44,61). After its release and action on P 2 receptors on vascular smooth muscle cells of the afferent arteriole, ATP would be rapidly metabolized to ADP, AMP, and ultimately adenosine by cell surface ectonucleotidase activity so that its effects would not be prolonged once secretion was terminated (21,87). The mechanism for the exocytotic release of ATP from macula densa cells remains unknown but could be similar to the Ca 2ϩ -dependent regulation of secretion seen in other cell types (69).…”

Section: Paracrine Mediators and Modulators Of Tgf Signalsmentioning

confidence: 58%

Integrating multiple paracrine regulators of renal microvascular dynamics

Navar

1998

American Journal of Physiology-Renal Physiology

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There has been tremendous growth in our knowledge about the multiple interacting mechanisms that regulate renal microvascular function. Paracrine signals originating from endothelial and epithelial cells exert profound influences on the basal tone and reactivity of the pre- and postglomerular arterioles. Selective responsiveness of these arterioles to various stimuli is possible because of differential activating mechanisms in vascular smooth muscle cells of afferent and efferent arterioles. Afferent arterioles rely predominantly on voltage-dependent calcium channels, while efferent arterioles utilize other mechanisms for calcium entry as well as intracellular calcium mobilization. The autoregulatory responses of preglomerular arterioles exemplify the selectivity of these complex control mechanisms. The myogenic mechanism responds to increases in renal perfusion pressure through “stretch-activated” cation channels that lead to depolarization, calcium entry, and vascular contraction. Autoregulatory efficiency is enhanced by the tubuloglomerular feedback (TGF) mechanism which responds to flow-dependent changes in tubular fluid composition at the level of the macula densa and transmits signals to the afferent arterioles to alter the activation state of voltage-dependent calcium channels. Recent studies have implicated extracellular ATP as one paracrine factor mediating TGF and autoregulatory related signals to the afferent arterioles. Other paracrine agents including nitric oxide, angiotensin II, adenosine, and arachidonic acid metabolites modulate vascular responsiveness in order to maintain an optimal balance between the metabolically determined reabsorptive capabilities of the tubules and the hemodynamically dependent filtered load.

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“…

The modulation by ATP of pre-synaptic ion channels (Zimmermann, 1994) via specific purinergic receptors, for example, could result in changes in subsequent release of neurotransmitters from the pre-synaptic site and, as a consequence, on the functional effect at the post-synaptic site.ATP is rapidly hydrolysed by ecto-nucleotidases (Gordon et al 1989) even at pre-synaptic sites (Thirion et al 1996) to adenosine 5‚-diphosphate (ADP), adenosine 5‚-monophosphate (AMP) and adenosine. Adenosine, the final hydrolysed metabolite of ATP (

…”

mentioning

confidence: 99%

“…ATP is rapidly hydrolysed by ecto-nucleotidases (Gordon et al 1989) even at pre-synaptic sites (Thirion et al 1996) to adenosine 5‚-diphosphate (ADP), adenosine 5‚-monophosphate (AMP) and adenosine. Adenosine, the final hydrolysed metabolite of ATP (…”

mentioning

confidence: 99%

Adenosine inhibition via A1 receptor of N-type Ca2+ current and peptide release from isolated neurohypophysial terminals of the rat

et al. 2002

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The modulation by ATP of pre-synaptic ion channels (Zimmermann, 1994) via specific purinergic receptors, for example, could result in changes in subsequent release of neurotransmitters from the pre-synaptic site and, as a consequence, on the functional effect at the post-synaptic site.ATP is rapidly hydrolysed by ecto-nucleotidases (Gordon et al. 1989) even at pre-synaptic sites (Thirion et al. 1996) to adenosine 5‚-diphosphate (ADP), adenosine 5‚-monophosphate (AMP) and adenosine. Adenosine, the final hydrolysed metabolite of ATP (

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The Hydrolysis of Extracellular Adenine Nucleotides by Arterial Smooth Muscle Cells

Cited by 91 publications

References 29 publications

Untitled

Untitled

Integrating multiple paracrine regulators of renal microvascular dynamics

Adenosine inhibition via A1 receptor of N-type Ca2+ current and peptide release from isolated neurohypophysial terminals of the rat

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