2001
DOI: 10.1253/jcj.65.451
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Role of Cardiac ATP-Sensitive K+ Channels Induced by Angiotensin II Type 1 Receptor Antagonist on Metabolism, Contraction and Relaxation in Ischemia-Reperfused Rabbit Heart.

Abstract: he renin-angiotensin system (RAS) plays an important role in the regulation of the cardiovascular system in various physiological or pathological conditions 1 and is activated on acute myocardial infarction both in humans 2 and in experimental animals. 3,4 Angiotensin II (Ang II) increases myocardial necrosis. 5 The localized Ang II exerts some deleterious effects on the myocardium of ischemia-reperfused heart. 6 Angiotensin II type 1 (AT1) receptor antagonists have the cardioprotective effect on ischemia-repe… Show more

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Cited by 9 publications
(5 citation statements)
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“…Activation of K ϩ channels also improves relaxation in failing myocardium. 29 Our in vivo human data show that levosimendan improves both cardiac contractility and relaxation in patients with heart failure. To our knowledge, this is the first catheterization laboratory-based study to assess changes in isovolumic relaxation in response to levosimendan.…”
Section: Lusitropic Effects Of Levosimendanmentioning
confidence: 76%
“…Activation of K ϩ channels also improves relaxation in failing myocardium. 29 Our in vivo human data show that levosimendan improves both cardiac contractility and relaxation in patients with heart failure. To our knowledge, this is the first catheterization laboratory-based study to assess changes in isovolumic relaxation in response to levosimendan.…”
Section: Lusitropic Effects Of Levosimendanmentioning
confidence: 76%
“…3 Intracellular Ca 2+ overload also leads to myocardial injury in ischemia -reperfusion [4][5][6][7][8] and the sarcolemmal Na + /Ca 2+ exchanger (NCX) is thought to be a major factor in the excessive Ca 2+ influx. 4,[6][7][8][9] Some previous reports have suggested that inhibition of the reverse mode of the NCX could protect ischemic myocardial cells against Ca 2+ overload, [7][8][9] but exchanger-related alterations in cytoplasmic Ca 2+ ([Ca 2+ ]i) and the effects of pharmacological intervention at the level of the NCX have not been fully described.…”
mentioning
confidence: 99%
“…Recently, we have demonstrated that the cardioprotective effect of combination of ACE inhibitor and AT1 receptor antagonist is not dependent on NO synthase in rabbit cardiac tissue (42). In addition, the cardioprotective effects of AT1 receptor antagonist in the stunned myocardium are provided by activation of KATP channels, which activation is mediated by the bradykinin B2 receptor via AT2 receptor activation (43).…”
Section: Discussionmentioning
confidence: 99%