| Role of blood flow in carotid body chemoreflex function in heart failure. | |
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MedLine Citation:
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PMID: 21078591 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Peripheral chemoreflex sensitivity is potentiated in clinical and experimental chronic heart failure (CHF). Blood supply to tissues is inevitably reduced in CHF. However, it remains poorly understood whether the reduced blood flow is the cause of increased peripheral chemoreflex sensitivity in CHF. This work highlights the effect of chronically reduced blood flow to the carotid body (CB) on peripheral chemoreflex function in rabbits. In pacing-induced CHF rabbits, blood flow in the carotid artery was reduced by 36.4 ± 5.2% after 3 weeks of pacing. For comparison, a similar level of blood flow reduction was induced by carotid artery occlusion (CAO) over a similar 3 week time course without pacing. CB blood supply was reduced by similar levels in both CHF and CAO rabbits as measured with fluorescent microspheres. Compared with sham rabbits, CAO enhanced peripheral chemoreflex sensitivity in vivo, increased CB chemoreceptor activity in an isolated CB preparation and decreased outward potassium current (Ik) in CB glomus cells to levels similar to those that were observed in CHF rabbits. In CAO CB compared to sham, neural nitric oxide (NO) synthase (nNOS) expression and NO levels were suppressed, and angiotensin II (Ang II) type 1 receptor (AT1-R) protein expression and Ang II concentration were elevated; these changes were similar to those seen in the CB from CHF rabbits. A NO donor and AT1-R antagonist reversed CAO-enhanced chemoreflex sensitivity. These results suggest that a reduction of blood flow to the CB is involved in the augmentation of peripheral chemoreflex sensitivity in CHF. |
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Authors:
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Yanfeng Ding; Yu-Long Li; Harold D Schultz |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-11-15 |
Journal Detail:
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Title: The Journal of physiology Volume: 589 ISSN: 1469-7793 ISO Abbreviation: J. Physiol. (Lond.) Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2011-01-12 Completed Date: 2011-04-22 Revised Date: 2012-01-02 |
Medline Journal Info:
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Nlm Unique ID: 0266262 Medline TA: J Physiol Country: England |
Other Details:
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Languages: eng Pagination: 245-58 Citation Subset: IM |
Affiliation:
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Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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metabolism Angiotensin II Type 1 Receptor Blockers / pharmacology Animals Blood Flow Velocity Cardiac Pacing, Artificial Carotid Arteries / innervation*, physiopathology*, surgery Carotid Body / drug effects, metabolism, physiopathology* Chemoreceptor Cells / drug effects, metabolism* Constriction Disease Models, Animal Heart Failure / etiology, metabolism, physiopathology* Kidney / innervation Male Nitric Oxide / metabolism Nitric Oxide Donors / pharmacology Nitric Oxide Synthase Type I / metabolism Potassium / metabolism Rabbits Receptor, Angiotensin, Type 1 / metabolism Reflex* / drug effects Regional Blood Flow Spectrometry, Fluorescence Sympathetic Nervous System / drug effects, physiopathology* Time Factors Ventricular Function, Left |
| Grant Support | |
ID/Acronym/Agency:
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P01-HL62222/HL/NHLBI NIH HHS; R01 HL098503-01A1/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Angiotensin II Type 1 Receptor Blockers; 0/Nitric Oxide Donors; 0/Receptor, Angiotensin, Type 1; 10102-43-9/Nitric Oxide; 11128-99-7/Angiotensin II; 7440-09-7/Potassium; EC 1.14.13.39/Nitric Oxide Synthase Type I |
| Comments/Corrections | |
Comment In:
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J Physiol. 2011 Feb 1;589(Pt 3):455-6
[PMID:
21285026
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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