Document Detail


Nitric oxide regulation of myocardial O2 consumption and HEP metabolism.
MedLine Citation:
PMID:  15374825     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
NO and O(2) compete at cytochrome-c oxidase, thus potentially allowing NO to modulate mitochondrial respiration. We previously observed a decrease of myocardial phosphocreatine (PCr)/ATP during very high cardiac work states, corresponding to an increase in cytosolic free ADP. This study tested the hypothesis that NO inhibition of respiration contributes to this increase of ADP. Infusion of dobutamine + dopamine (DbDp, each 20 microg.kg(-1).min(-1) iv) to more than double myocardial oxygen consumption (MVo(2)) in open-chest dogs caused a decrease of myocardial PCr/ATP measured with (31)P NMR from 2.04 +/- 0.09 to 1.85 +/- 0.08 (P < 0.05). Inhibition of NO synthesis with N(omega)-nitro-L-arginine (L-NNA), while catecholamine infusion continued, caused PCr/ATP to increase to the control value. In a second group of animals, L-NNA administered before catecholamine stimulation (reverse intervention of the first group) increased PCr/ATP during basal conditions. In these animals L-NNA did not prevent a decrease of PCr/ATP at the high cardiac work state but, relative to MVo(2), PCr/ATP was significantly higher after L-NNA. In a third group of animals, pharmacological coronary vasodilation with carbochromen was used to prevent changes in coronary flow that might alter endothelial NO production. In these animals L-NNA again restored depressed myocardial PCr/ATP during catecholamine infusion. The finding that inhibition of NO production increased PCr/ATP suggests that during very high work states NO inhibition of mitochondrial respiration requires ADP to increase to drive oxidative phosphorylation.
Authors:
Jianyi Zhang; Guangrong Gong; Yun Ye; Tao Guo; Abdul Mansoor; Qingsong Hu; Koichi Ochiai; Jingbo Liu; Xiaohong Wang; Yarong Cheng; Nicole Iverson; Joseph Lee; Arthur H L From; Kamil Ugurbil; Robert J Bache
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2004-09-16
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  288     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2005 Jan 
Date Detail:
Created Date:  2004-12-15     Completed Date:  2005-03-22     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H310-6     Citation Subset:  IM    
Affiliation:
Department of Medicine, Center for Magnetic Resonance Research, University of Minnesota, Minneapolis, MN 55455, USA. zhang047@umn.edu
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MeSH Terms
Descriptor/Qualifier:
Adenosine Diphosphate / metabolism*
Animals
Dogs
Energy Metabolism / physiology*
Female
Magnetic Resonance Spectroscopy
Male
Myocardium / metabolism*
Nitric Oxide / physiology*
Oxygen Consumption / physiology*
Phosphocreatine / metabolism*
Grant Support
ID/Acronym/Agency:
HL-20598/HL/NHLBI NIH HHS; HL-21872/HL/NHLBI NIH HHS; HL-33600/HL/NHLBI NIH HHS; HL-50470/HL/NHLBI NIH HHS; HL-58840/HL/NHLBI NIH HHS; HL-61353/HL/NHLBI NIH HHS; HL-67828/HL/NHLBI NIH HHS; HL-71970/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
10102-43-9/Nitric Oxide; 58-64-0/Adenosine Diphosphate; 67-07-2/Phosphocreatine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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