| ATP hydrolysis pathways and their contributions to pial arteriolar dilation in rats. | |
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MedLine Citation:
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PMID: 21803949 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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ATP is thought to be released to the extracellular compartment by neurons and astrocytes during neural activation. We examined whether ATP exerts its effect of promoting pial arteriolar dilation (PAD) directly or upon conversion (via ecto-nucleotidase action) to AMP and adenosine. Blockade of extracellular direct ATP to AMP conversion, with ARL-67156, significantly reduced sciatic nerve stimulation-evoked PADs by 68%. We then monitored PADs during suffusions of ATP, ADP, AMP, and adenosine in the presence and absence of the following: 1) the ecto-5'-nucleotidase inhibitor α,β-methylene adenosine 5'-diphosphate (AOPCP), 2) the A(2) receptor blocker ZM 241385, 3) the ADP P2Y(1) receptor antagonist MRS 2179, and 4) ARL-67156. Vasodilations induced by 1 and 10 μM, but not 100 μM, ATP were markedly attenuated by ZM 241385, AOPCP, and ARL-67156. Substantial loss of reactivity to 100 μM ATP required coapplications of ZM 241385 and MRS 2179. Dilations induced by ADP were blocked by MRS 2179 but were not affected by either ZM 241385 or AOPCP. AMP-elicited dilation was partially inhibited by AOPCP and completely abolished by ZM 241385. Collectively, these and previous results indicate that extracellular ATP-derived adenosine and AMP, via A(2) receptors, play key roles in neural activation-evoked PAD. However, at high extracellular ATP levels, some conversion to ADP may occur and contribute to PAD through P2Y(1) activation. |
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Authors:
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Francesco Vetri; Haoliang Xu; Lizhen Mao; Chanannait Paisansathan; Dale A Pelligrino |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-07-29 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 301 ISSN: 1522-1539 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2011 Oct |
Date Detail:
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Created Date: 2011-09-29 Completed Date: 2011-11-22 Revised Date: 2013-02-08 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1369-77 Citation Subset: IM |
Affiliation:
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Neuroanesthesia Research, University of Illinois at Chicago, Chicago, Illinois 60612, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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5'-Nucleotidase
/
antagonists & inhibitors,
metabolism Adenosine A2 Receptor Antagonists / pharmacology Adenosine Triphosphate / analogs & derivatives, metabolism, pharmacology, physiology* Animals Antigens, CD / metabolism Apyrase / antagonists & inhibitors, metabolism Arterioles / physiology Carbon Dioxide / metabolism Dose-Response Relationship, Drug Electric Stimulation Female Hydrolysis Indicators and Reagents Purinergic P2Y Receptor Antagonists / pharmacology Rats Rats, Sprague-Dawley Receptors, Purinergic P1 / drug effects Receptors, Purinergic P2Y1 / drug effects Sciatic Nerve / physiology Vasodilation / physiology* |
| Grant Support | |
ID/Acronym/Agency:
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HL-088259/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/6-N,N-diethyl-beta,gamma-dibromomethylene-D-ATP; 0/Adenosine A2 Receptor Antagonists; 0/Antigens, CD; 0/Indicators and Reagents; 0/Purinergic P2Y Receptor Antagonists; 0/Receptors, Purinergic P1; 0/Receptors, Purinergic P2Y1; 124-38-9/Carbon Dioxide; 56-65-5/Adenosine Triphosphate; EC 3.1.3.5/5'-Nucleotidase; EC 3.6.1.5/Apyrase; EC 3.6.1.5/CD39 antigen |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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