| Oxygen sensing and conducted vasomotor responses in mouse cremaster arterioles in situ. | |
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MedLine Citation:
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PMID: 20383716 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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This study examines mechanisms by which changes in tissue oxygen tension elicit vasomotor responses and whether localized changes in oxygen tension initiates conducted vasomotor responses in mouse cremaster arterioles. Intravital microscopy was used to visualize the mouse cremaster microcirculation. The cremaster was superfused with Krebs' solution with different oxygen tensions, and a gas exchange chamber was used to induce localized changes in oxygen tension. In arterioles where red blood cells were removed by buffer perfusion, arterioles responded with same magnitudes of vasodilatation (DeltaD = 16.0 +/- 4.9 microm) when changing from high (PO(2) = 242.5 +/- 13.3 mm Hg) to low (PO(2) = 22.5 +/- 4.8 mm Hg) oxygen tension as seen in the intact cremaster circulation (DeltaD = 18.7 +/- 1.0 microm). Blockade of NO synthases by L: -NAME and adenosine receptors by DPCPX had no effects on vasomotor responses to low or high oxygen. Induction of localized low (PO(2) = 23.3 +/- 5.7 mmHg) or high (PO(2) = 300.0 +/- 25.7 mm Hg) oxygen tension caused vasodilatation or -constriction locally and at a site 1,000 microm upstream (distantly). Glibenclamide blocker of ATP-sensitive K(+) channels inhibited vasodilatation and -constriction to low (PO(2) = 16.0 +/- 6.4 mm Hg) and high (PO(2) = 337.4 +/- 12.8 mm Hg) oxygen tension. 1) ATP-sensitive K(+) channels seem to mediate, at least in part, vasodilatation and vasoconstriction to low and high oxygen tension; 2) Red blood cells are not necessary for inducing vasodilatation and vasoconstriction to low or high oxygen tension; 3) localized changes in the oxygen tension cause vasomotor responses, which are conducted upstream along arterioles in mouse cremaster microcirculation. |
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Authors:
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Anh Thuc Ngo; Lars Jørn Jensen; Mads Riemann; Niels-Henrik Holstein-Rathlou; Christian Torp-Pedersen |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-04-11 |
Journal Detail:
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Title: Pflügers Archiv : European journal of physiology Volume: 460 ISSN: 1432-2013 ISO Abbreviation: Pflugers Arch. Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-05-18 Completed Date: 2010-08-24 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0154720 Medline TA: Pflugers Arch Country: Germany |
Other Details:
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Languages: eng Pagination: 41-53 Citation Subset: IM |
Affiliation:
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Division of Renal & Vascular Research, Department of Biomedical Sciences, University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen, Denmark. anhngo@sund.ku.dk |
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine
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metabolism Animals Arterioles / injuries, metabolism Cell Hypoxia Enzyme Inhibitors / pharmacology Erythrocytes / metabolism KATP Channels / antagonists & inhibitors, metabolism Male Mice Mice, Inbred C57BL Microcirculation Microscopy, Video Muscles / blood supply* Nitric Oxide / metabolism Nitric Oxide Synthase / antagonists & inhibitors, metabolism Oxygen / blood, metabolism* Perfusion Potassium Channel Blockers / pharmacology Receptor, Adenosine A1 / antagonists & inhibitors, metabolism Receptors, Adenosine A2 / antagonists & inhibitors, metabolism Regional Blood Flow Vasoconstriction* / drug effects Vasodilation* / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; 0/KATP Channels; 0/Potassium Channel Blockers; 0/Receptor, Adenosine A1; 0/Receptors, Adenosine A2; 10102-43-9/Nitric Oxide; 58-61-7/Adenosine; 7782-44-7/Oxygen; EC 1.14.13.39/Nitric Oxide Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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