Document Detail

Effects of an HMG-CoA reductase inhibitor in combination with an ACE inhibitor or angiotensin II type 1 receptor antagonist on myocardial metabolism in ischemic rabbit hearts.
MedLine Citation:
PMID:  12047036     Owner:  NLM     Status:  MEDLINE    
We investigated the effects of a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, pravastatin, an angiotensin converting enzyme (ACE) inhibitor, temocaprilat, and an angiotensin II type 1 (AT1) receptor antagonist, CV-11974, on myocardial metabolism during ischemia in isolated rabbit hearts using phosphorus 31-nuclear magnetic resonance (31P-NMR) imaging. Forty-five minutes of continuous normothermic global ischemia was carried out. Pravastatin, temocaprilat, CV-11974 or a nitric oxide synthase inhibitor, L-NAME was administered from 60 min prior to the global ischemia. Japanese white rabbits were divided into the following experimental groups, a control group (n=7), a group treated with pravastatin (P group; n=7), a group treated with pravastatin and temocaprilat (P+T group; n=7), a group treated with pravastatin and CV-11974 (P+CV group; n=7), and a group treated with pravastatin and L-NAME (P+L-NAME group; n=7). During ischemia, P group, as well as either P+T group or P+CV group, showed a significant inhibition of the decreases in adenosine triphosphate (ATP) and intracellular pH (pHi) (p<0.01, respectively, at the end of ischemia compared to the control group as well as P+L-NAME group), and a significant inhibition of the increase in inorganic phosphate (Pi) (p<0.01, respectively, compared with the control group as well as P+L-NAME group). These results suggest that pravastatin significantly improved myocardial energy metabolism during myocardial ischemia. This beneficial effect was dependent on NO synthase. However, this beneficial effect was not enhanced by either temocaprilat or CV-11974.
Hitoshi Kawabata; Kizuku Nakagawa; Kinji Ishikawa
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Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  Hypertension research : official journal of the Japanese Society of Hypertension     Volume:  25     ISSN:  0916-9636     ISO Abbreviation:  Hypertens. Res.     Publication Date:  2002 Mar 
Date Detail:
Created Date:  2002-06-05     Completed Date:  2002-11-13     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  9307690     Medline TA:  Hypertens Res     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  203-10     Citation Subset:  IM    
First Department of Internal Medicine, Kinki University School of Medicine, Osakasayama, Japan.
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MeSH Terms
Adenosine Triphosphate / metabolism
Angiotensin Receptor Antagonists*
Angiotensin-Converting Enzyme Inhibitors / pharmacology*
Antihypertensive Agents / pharmacology
Benzimidazoles / pharmacology
Cardiotonic Agents / pharmacology
Drug Combinations
Enzyme Inhibitors / pharmacology
Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
Myocardial Ischemia / metabolism*
Myocardium / metabolism*
NG-Nitroarginine Methyl Ester / pharmacology
Phosphates / metabolism
Pravastatin / pharmacology
Receptor, Angiotensin, Type 1
Tetrazoles / pharmacology
Thiazepines / pharmacology
Reg. No./Substance:
0/Angiotensin Receptor Antagonists; 0/Angiotensin-Converting Enzyme Inhibitors; 0/Antihypertensive Agents; 0/Benzimidazoles; 0/Cardiotonic Agents; 0/Drug Combinations; 0/Enzyme Inhibitors; 0/Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0/Phosphates; 0/Receptor, Angiotensin, Type 1; 0/Tetrazoles; 0/Thiazepines; 110221-53-9/temocaprilat; 50903-99-6/NG-Nitroarginine Methyl Ester; 56-65-5/Adenosine Triphosphate; 81093-37-0/Pravastatin; S8Q36MD2XX/candesartan

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

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