Document Detail


Interstitial norepinephrine concentrations in skeletal muscle of ischemic heart failure.
MedLine Citation:
PMID:  17449553     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Jihong Xing; Satoshi Koba; Valerie Kehoe; Zhaohui Gao; Kristen Rice; Nicholas King; Lawrence Sinoway; Jianhua Li
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural     Date:  2007-04-20
Journal Detail:
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:
Created Date:  2007-08-03     Completed Date:  2007-09-18     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1190-5     Citation Subset:  IM    
Affiliation:
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.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic Uptake Inhibitors / 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:
R01 HL060800/HL/NHLBI NIH HHS; R01 HL075533/HL/NHLBI NIH HHS; R01 HL078866/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic Uptake Inhibitors; 0/Norepinephrine Plasma Membrane Transport Proteins; 0/Slc6a2 protein, rat; 50-47-5/Desipramine; 51-41-2/Norepinephrine

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