NTPDase1 (CD39) controls nucleotide-dependent vasoconstriction in mouse

Kauffenstein, Gilles; Drouin, Annick; Thorin‐Trescases, Nathalie; Bachelard, Hélène; Robaye, Bernard; D’Orléans-Juste, Pedro; Marceau, François; Thorin, Éric; Sévigny, Jean

doi:10.1093/cvr/cvp265

Cited by 91 publications

(93 citation statements)

References 48 publications

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“…Pharmacological [272] or pathological [119] manoeuvres that impair P2X1 receptor signalling will also blunt whole kidney autoregulation of blood flow, both in vivo and in vitro. Finally, mice with a targeted deletion of the ectonucleotidase NTPDase1 exhibit enhanced pressureinduced vasoconstriction in the mesenteric artery [183]. This probably reflects the prolonged half-life of extracellular ATP and is consistent with a key role for local nucleotide signalling in the general myogenic response.…”

Section: Myogenic Responses To Altered Perfusion Pressuresupporting

confidence: 55%

Purinergic signalling in the kidney in health and disease

Burnstock

Evans

Bailey

2013

Purinergic Signalling

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The involvement of purinergic signalling in kidney physiology and pathophysiology is rapidly gaining recognition and this is a comprehensive review of early and recent publications in the field. Purinergic signalling involvement is described in several important intrarenal regulatory mechanisms, including tuboglomerular feedback, the autoregulatory response of the glomerular and extraglomerular microcirculation and the control of renin release. Furthermore, purinergic signalling influences water and electrolyte transport in all segments of the renal tubule. Reports about purine-and pyrimidine-mediated actions in diseases of the kidney, including polycystic kidney disease, nephritis, diabetes, hypertension and nephrotoxicant injury are covered and possible purinergic therapeutic strategies discussed.

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Section: Myogenic Responses To Altered Perfusion Pressuresupporting

confidence: 55%

Purinergic signalling in the kidney in health and disease

Burnstock

Evans

Bailey

2013

Purinergic Signalling

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“…It furthermore controls endothelial P2Y receptor-dependent vasorelaxation [49]. In addition, NTPDase1 is the major enzyme regulating nucleotide metabolism at the surface of vascular smooth muscle cells and thus contributes to the local regulation of vascular tone by nucleotides [49,50]. Enzymes capable of the specified catalytic reaction are highlighted with a colored background box.…”

Section: General Properties and Functional Rolementioning

confidence: 99%

Cellular function and molecular structure of ecto-nucleotidases

Zimmermann

Zebisch

Sträter

2012

Purinergic Signalling

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922

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Ecto-nucleotidases play a pivotal role in purinergic signal transmission. They hydrolyze extracellular nucleotides and thus can control their availability at purinergic P2 receptors. They generate extracellular nucleosides for cellular reuptake and salvage via nucleoside transporters of the plasma membrane. The extracellular adenosine formed acts as an agonist of purinergic P1 receptors. They also can produce and hydrolyze extracellular inorganic pyrophosphate that is of major relevance in the control of bone mineralization. This review discusses and compares four major groups of ectonucleotidases: the ecto-nucleoside triphosphate diphosphohydrolases, ecto-5′-nucleotidase, ecto-nucleotide pyrophosphatase/phosphodiesterases, and alkaline phosphatases. Only recently and based on crystal structures, detailed information regarding the spatial structures and catalytic mechanisms has become available for members of these four ecto-nucleotidase families. This permits detailed predictions of their catalytic mechanisms and a comparison between the individual enzyme groups. The review focuses on the principal biochemical, cell biological, catalytic, and structural properties of the enzymes and provides brief reference to tissue distribution, and physiological and pathophysiological functions.

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“…Commercially available ligands do not discriminate well between P2Y 2 and P2Y 4 receptors, and the default position is that one or both are expressed in tissues where responses to UTP (P2Y 2/4 agonist, weak P2Y 6 agonist) are demonstrated. However, the use of P2Y 6 receptor knockouts showed that the contractile response to UTP in mouse aorta was mediated via P2Y 6 receptors and not via P2Y 2 receptors, which were shown by RT-PCR to be expressed in the smooth muscle (Bar et al, 2008;Kauffenstein et al, 2010a). Similarly, the use of knockouts and antisense oligonucleotides showed the functional expression of vasocontractile P2Y 4 and P2Y 6 but not P2Y 2 receptors in mouse mesenteric arteries and cerebral arterioles (Vial and Evans, 2002;Bar et al, 2008;Kauffenstein et al, 2010a;Brayden et al, 2013).…”

Section: Introductionmentioning

confidence: 99%