Document Detail

Mitochondrial aldehyde dehydrogenase mediates vasodilator responses of glyceryl trinitrate and sodium nitrite in the pulmonary vascular bed of the rat.
MedLine Citation:
PMID:  20543077     Owner:  NLM     Status:  MEDLINE    
It has been reported that mitochondrial aldehyde dehydrogenase (ALDH2) catalyzes the formation of glyceryl dinitrate and inorganic nitrite from glyceryl trinitrate (GTN), leading to an increase in cGMP and vasodilation in the coronary and systemic vascular beds. However, the role of nitric oxide (NO) formed from nitrite in mediating the response to GTN in the pulmonary vascular bed is uncertain. The purpose of the present study was to determine if nitrite plays a role in mediating vasodilator responses to GTN. In this study, intravenous injections of GTN and sodium nitrite decreased pulmonary and systemic arterial pressures and increased cardiac output. The decreases in pulmonary arterial pressure under baseline and elevated tone conditions and decreases in systemic arterial pressure in response to GTN and sodium nitrite were attenuated by cyanamide, an ALDH2 inhibitor, whereas responses to the NO donor, sodium nitroprusside (SNP), were not altered. The decreases in pulmonary and systemic arterial pressure in response to GTN and SNP were not altered by allopurinol, an inhibitor of xanthine oxidoreductase, whereas responses to sodium nitrite were attenuated. GTN was approximately 1,000-fold more potent than sodium nitrite in decreasing pulmonary and systemic arterial pressures. These results suggest that ALDH2 plays an important role in the bioactivation of GTN and nitrite in the pulmonary and systemic vascular beds and that the reduction of nitrite to vasoactive NO does not play an important role in mediating vasodilator responses to GTN in the intact chest rat.
Adeleke M Badejo; Chris Hodnette; Jasdeep S Dhaliwal; David B Casey; Edward Pankey; Subramanyam N Murthy; Bobby D Nossaman; Albert L Hyman; Philip J Kadowitz
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-06-11
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-31     Completed Date:  2010-09-22     Revised Date:  2011-09-13    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H819-26     Citation Subset:  IM    
Department of Pharmacology, Tulane University School of Medicine, New Orleans 70112-2699, USA.
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MeSH Terms
Aldehyde Dehydrogenase / metabolism*
Analysis of Variance
Cyanamide / pharmacology
Enzyme Inhibitors / pharmacology
Lung / blood supply*,  drug effects,  metabolism
Mitochondria / drug effects,  metabolism*
Mitochondrial Proteins / metabolism*
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide / metabolism
Nitroglycerin / metabolism*,  pharmacology
Pulmonary Circulation / drug effects,  physiology
Rats, Sprague-Dawley
Sodium Nitrite / metabolism*,  pharmacology
Vasodilation / drug effects,  physiology*
Vasodilator Agents / pharmacology
Grant Support
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Mitochondrial Proteins; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 420-04-2/Cyanamide; 50903-99-6/NG-Nitroarginine Methyl Ester; 55-63-0/Nitroglycerin; 7632-00-0/Sodium Nitrite; EC Dehydrogenase; EC protein, rat

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

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