| Interstitial norepinephrine concentrations in skeletal muscle of ischemic heart failure. | |
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MedLine Citation:
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PMID: 17449553 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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During exercise, sympathetic nerve responses are accentuated in heart failure (HF), and this enhances norepinephrine (NE) release and evokes vasoconstriction. Two key pathophysiological responses could contribute to the greater NE release: 1) increased sympathetic nerve discharge and 2) increased NE in the neurovascular junction for a given level of sympathetic discharge. In this report, we focus on the second of these two general issues and test the following hypotheses: 1) in HF for a given level of sympathetic nerve stimulation, NE concentration in the interstitium (an index of neurovascular NE) would be greater, and 2) the greater interstitial NE concentration would be linked to reduced NE uptake. Studies were performed in rats 8-10 wk after induction of myocardial infarction (MI). Interstitial NE samples were collected from microdialysis probes inserted into the hindlimb muscle. Dialysate concentration of NE was determined by the HPLC method. First, interstitial NE concentration increased during electrical stimulation of the lumbar sympathetic nerves in eight control rats. An increase in interstitial NE concentration was significantly greater in 10 rats with severe MI. Additionally, an NE uptake-1 inhibitor (desipramine, 1 microM) was injected into the arterial blood supply of the muscle in six control and eight MI rats. Desipramine increased interstitial NE concentration by 24% in control and by only 3% (P < 0.05 vs. control) in MI rats. In conclusion, given levels of electrical stimulation of the lumbar sympathetic nerve lead to higher interstitial NE concentration in HF. This effect is due, in part, to reduced NE uptake-1 in HF. |
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Authors:
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Jihong Xing; Satoshi Koba; Valerie Kehoe; Zhaohui Gao; Kristen Rice; Nicholas King; Lawrence Sinoway; Jianhua Li |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural Date: 2007-04-20 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 293 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2007 Aug |
Date Detail:
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Created Date: 2007-08-03 Completed Date: 2007-09-18 Revised Date: 2007-12-03 |
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: H1190-5 Citation Subset: IM |
Affiliation:
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Penn State Heart and Vascular Institute, The Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, 500 Univ. Dr., Hershey, PA 17033, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adrenergic Uptake Inhibitors
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pharmacology Animals Cardiac Output, Low / etiology, metabolism*, physiopathology Chromatography, High Pressure Liquid Coronary Vessels / surgery Desipramine / pharmacology Disease Models, Animal Electric Stimulation / methods Extracellular Fluid / metabolism* Hindlimb Ligation Lumbosacral Plexus / metabolism Male Microdialysis Muscle, Skeletal / drug effects, innervation, metabolism* Myocardial Infarction / complications*, etiology, metabolism, physiopathology Myocardial Ischemia / complications*, metabolism, physiopathology Norepinephrine / metabolism* Norepinephrine Plasma Membrane Transport Proteins / antagonists & inhibitors, metabolism Rats Rats, Sprague-Dawley Severity of Illness Index Sympathetic Nervous System / drug effects, metabolism*, physiopathology Ventricular Function, Left |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL060800/HL/NHLBI NIH HHS; R01 HL075533/HL/NHLBI NIH HHS; R01 HL078866/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Adrenergic Uptake Inhibitors; 0/Norepinephrine Plasma Membrane Transport Proteins; 0/Slc6a2 protein, rat; 50-47-5/Desipramine; 51-41-2/Norepinephrine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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