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Titolo:
Role of cardiac ATP-sensitive K+ channels induced by HMG CoA reductase inhibitor in ischemic rabbit hearts
Autore:
Kawabata, H; Ryomoto, T; Ishikawa, K;
Indirizzi:
Kinki Univ, Sch Med, Dept Internal Med 1, Osakasayama, Osaka 5898511, Japan Kinki Univ Osakasayama Osaka Japan 5898511 kasayama, Osaka 5898511, Japan
Titolo Testata:
Hypertension research
fascicolo: 5, volume: 24, anno: 2001,
pagine: 573 - 577
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; DEPENDENT POTASSIUM CHANNELS; REPERFUSION INJURY; INFARCT SIZE; L-ARGININE; MITOCHONDRIAL; PRAVASTATIN; CARDIOPROTECTION; INVOLVEMENT; MYOCYTES;
Keywords:
ATP-sensitive channel; HMG-CoA reductase inhibitor; nitric oxide; cardioprotection; ischemia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Kawabata, H Kinki Univ, Sch Med, Dept Internal Med 1, 377-2 Ohnohigashi, Osakasayama, Osaka 5898511, Japan Kinki Univ 377-2 Ohnohigashi Osakasayama Osaka Japan 5898511 n
Citazione:
H. Kawabata et al., "Role of cardiac ATP-sensitive K+ channels induced by HMG CoA reductase inhibitor in ischemic rabbit hearts", HYPERTENS R, 24(5), 2001, pp. 573-577

Abstract

Although 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors can protect the myocardium against ischemic injury, the mechanisms of their effect have not yet been characterized at the cellular level. Therefore, we investigated the role of cardiac ATP-sensitive K+ (K-ATP) channels induced by the HMG-CoA reductase inhibitor known as pravastatin on the myocardial metabolism during ischemia by phosphorus 31-nuclear magnetic resonance(P-31-NMR) in isolated rabbit hearts. Forty-five min of continuous normothermic global ischemia was carried out. Pravastatin with or without the K-ATP channel blocker glibenclamide or the nitric oxide synthase inhibitor L-NAME was administered beginning 60 min prior to the global ischemia. Twenty-eight hearts were divided into 4 experimental groups consisting of 7 hearts each: the control group, the P group consisting of pravastatin treatment, the P + G group consisting of pravastatin treatment with glibenclamide, and the P + L group consisting of pravastatin treatment with L-NAME. During ischemia, the decreases in adenosine triphosphate (ATP) and intracellular pH (pHi) were significantly inhibited in the P group in comparison with Controlgroup (at end of ischemia, respectively; both p < 0.01), as was the increase in inorganic phosphate (Pi) (at end of ischemia, p < 0.01). However, thedecreases in ATP and pHi and the increase in Pi were not inhibited in the P + G group during ischemia. The P + L group also showed no inhibition of the aforementioned parameters during the same period. These results suggest that pravastatin has a significant beneficial effect for improving the myocardial energy metabolism, which is provided by K-ATP channels and nitric oxide (NO), during myocardial ischemia. The cardioprotection of HMG-CoA reductase inhibitor may be caused by the K-ATP channels that are mediated by theNO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 21:44:10