Nicorandil Protects Against Lethal Ischemic Ventricular Arrhythmias and Up-regulates Endothelial Nitric Oxide Synthase Expression and Sulfonylurea Receptor 2 mRNA in Conscious Rats with Acute Myocardial Infarction

[1]  Y. Hattori,et al.  Pyrrolidine dithiocarbamate inhibits cytokine-induced VCAM-1 gene expression in rat cardiac myocytes , 1997, Molecular and Cellular Biochemistry.

[2]  M. Kinoshita,et al.  Mechanism of the vasodilatory action of nicorandil on coronary circulation in dogs , 1994, Cardiovascular Drugs and Therapy.

[3]  W. Hillis,et al.  Effect of nicorandil on coronary events in patients with stable angina: the Impact Of Nicorandil in Angina (IONA) randomised trial , 2002, The Lancet.

[4]  B. Das,et al.  Selective mitochondrial K(ATP) channel activation results in antiarrhythmic effect during experimental myocardial ischemia/reperfusion in anesthetized rabbits. , 2002, European journal of pharmacology.

[5]  N. Kobayashi,et al.  Nicorandil Enhances Cardiac Endothelial Nitric Oxide Synthase Expression via Activation of Adenosine Triphosphate‐Sensitive K Channel in Rat , 2001, Journal of cardiovascular pharmacology.

[6]  J. Pernow,et al.  Involvement of nitric oxide in cardioprotective effect of endothelin receptor antagonist during ischemia-reperfusion. , 2001, American journal of physiology. Heart and circulatory physiology.

[7]  S. Sasayama,et al.  Differential expression of three types of nitric oxide synthase in both infarcted and non-infarcted left ventricles after myocardial infarction in the rat. , 2000, International journal of cardiology.

[8]  D. Yellon,et al.  Infarct size and nitric oxide synthase in murine myocardium. , 2000, Journal of molecular and cellular cardiology.

[9]  N. Kobayashi,et al.  Benidipine stimulates nitric oxide synthase and improves coronary circulation in hypertensive rats. , 1999, American journal of hypertension.

[10]  Y. Taniyama,et al.  Intravenous nicorandil can preserve microvascular integrity and myocardial viability in patients with reperfused anterior wall myocardial infarction. , 1999, Journal of the American College of Cardiology.

[11]  赤尾 昌治.  Myocardial ischemia induces differential regulation of K[ATP] channel gene expression in rat hearts , 1999 .

[12]  Y. Horio,et al.  SUR2 subtype (A and B)‐dependent differential activation of the cloned ATP‐sensitive K+ channels by pinacidil and nicorandil , 1998, British journal of pharmacology.

[13]  大野嘉嗣.  Nicorandil reduces myocardial infarct size by opening the K[ATP] channel in rabbits , 1998 .

[14]  M. Horie,et al.  Myocardial ischemia induces differential regulation of KATP channel gene expression in rat hearts. , 1997, The Journal of clinical investigation.

[15]  M. Hori,et al.  Salutary effect of adjunctive intracoronary nicorandil administration on restoration of myocardial blood flow and functional improvement in patients with acute myocardial infarction. , 1997, American heart journal.

[16]  G. Gross,et al.  Glibenclamide-induced blockade of ischemic preconditioning is time dependent in intact rat heart. , 1997, The American journal of physiology.

[17]  G. Grover.  Pharmacology of ATP-sensitive potassium channel (KATP) openers in models of myocardial ischemia and reperfusion. , 1997, Canadian journal of physiology and pharmacology.

[18]  T. Yoshimoto,et al.  Gene expression of endothelial type isoform of nitric oxide synthase in various tissues of stroke-prone spontaneously hypertensive rats. , 1997, Hypertension research : official journal of the Japanese Society of Hypertension.

[19]  Wu Song,et al.  Delayed protection against ischaemia‐induced ventricular arrhythmias and infarct size limitation by the prior administration of Escherichia coli endotoxin , 1996, British journal of pharmacology.

[20]  J. Papp,et al.  ATP-sensitive potassium channel modulators: both pinacidil and glibenclamide produce antiarrhythmic activity during acute myocardial infarction in conscious rats. , 1996, The Journal of pharmacology and experimental therapeutics.

[21]  N. Kobayashi,et al.  Effect of trichlormethiazide and captopril on nitric oxide synthase activity in the kidney of deoxycorticosterone acetate-salt hypertensive rats. , 1996, Japanese heart journal.

[22]  G. Gross,et al.  Bimakalim, an ATP-sensitive potassium channel opener, mimics the effects of ischemic preconditioning to reduce infarct size, adenosine release, and neutrophil function in dogs. , 1995, Circulation.

[23]  J. M. Di Diego,et al.  Pinacidil-induced electrical heterogeneity and extrasystolic activity in canine ventricular tissues. Does activation of ATP-regulated potassium current promote phase 2 reentry? , 1993, Circulation.

[24]  Y. Hattori,et al.  GTP cyclohydrolase I mRNA is induced by LPS in vascular smooth muscle: characterization, sequence and relationship to nitric oxide synthase. , 1993, Biochemical and biophysical research communications.

[25]  N. Ishida,et al.  Cloning of inducible nitric oxide synthase in rat vascular smooth muscle cells. , 1993, Biochemical and biophysical research communications.

[26]  F. Marumo,et al.  Polymerase chain reaction localization of constitutive nitric oxide synthase and soluble guanylate cyclase messenger RNAs in microdissected rat nephron segments. , 1992, The Journal of clinical investigation.

[27]  P. Kubes,et al.  Nitric oxide: an endogenous modulator of leukocyte adhesion. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[28]  N. Taira,et al.  Nicorandil as a hybrid between nitrates and potassium channel activators. , 1989, The American journal of cardiology.

[29]  S. Moncada,et al.  Vascular endothelial cells synthesize nitric oxide from L-arginine , 1988, Nature.

[30]  P. Chomczyński,et al.  Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. , 1987, Analytical biochemistry.

[31]  S. Holzmann.  Cyclic GMP as Possible Mediator of Coronary Arterial Relaxation by Nicorandil (SG‐75) , 1983, Journal of cardiovascular pharmacology.

[32]  J. Parratt,et al.  Coronary artery ligation in anesthetized rats as a method for the production of experimental dysrhythmias and for the determination of infarct size. , 1980, Journal of pharmacological methods.