Roles of mitochondrial ATP-sensitive K channels and PKC in anti-infarct tolerance afforded by adenosine A1receptor activation

Miura, Tetsuji; Liu, Yongge; Kita, Hidefumi; Ogawa, Takashi; Shimamoto, Kazuaki

doi:10.1016/s0735-1097(99)00493-3

Cited by 104 publications

(75 citation statements)

References 34 publications

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“…[32][33][34] The mechanisms by which IP inhibits reperfusion arrhythmias may involve the reduction of Ca 2+ overload due to the inhibition of production of [H + ] and lactate [35][36][37] and the opening of sarcolemmal and/or mitochondrial K ATP channels. [38][39][40][41][42][43][44] However, the details of the mechanisms have not been clarified. In control rats, the incidence and the duration of RVT in CIP(+) were significantly lower than in CIP(-)(P < 0.05).…”

Section: Discussionmentioning

confidence: 99%

The Insulin Sensitizer Pioglitazone Improves the Deterioration of Ischemic Preconditioning in Type 2 Diabetes Mellitus Rats

et al. 2007

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SUMMARYWe investigated the effects of ischemic preconditioning (IP) on reperfusion arrhythmias in type 2 diabetic rats as well as the effects of the insulin sensitizer pioglitazone. Thirty-week-old OLETF rats with or without pioglitazone (10 mg/kgBW, orally) were used as a model for type 2 diabetes. LETO rats served as controls. The incidences and durations of reperfusion ventricular tachyarrhythmias (RVT) were evaluated using a working heart method. After 5 minutes of initial perfusion, the rats were divided into the following groups: 1) control rats without IP (CIP(-)), 2) control rats with IP (CIP(+)), 3) diabetic rats without IP (DIP(-)), 4) diabetic rats with IP (DIP(+)), 5) pioglitazone-treated diabetic rats without IP (TDIP(-)), and 6) pioglitazone-treated diabetic rats with IP (TDIP(+)). Three 2-minute cycles of global diastolic ischemia and 5 minutes of reperfusion before long ischemia were performed as IP. The incidence and duration of RVT in CIP(+) were significantly lower than in CIP(-). There was no significant difference in the duration of RVT between DIP(+) and DIP(-). However, the duration of RVT in TDIP(+) was significantly shorter than TDIP(-). These results suggested that the effects of IP on reperfusion arrhythmias are deteriorated in type 2 diabetic rats. The insulin sensitizer pioglitazone can improve the deterioration of IP against reperfusion arrhythmias in type 2 diabetic rats. (Int Heart J 2007; 48: 623-635)

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Section: Discussionmentioning

confidence: 99%

The Insulin Sensitizer Pioglitazone Improves the Deterioration of Ischemic Preconditioning in Type 2 Diabetes Mellitus Rats

et al. 2007

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“…However, Sanada et al showed that in a dog model, the sarcolemmal and mito-KATP channels were equally important in reducing infarct size. 19 The species difference should be noted and we should be careful in extrapolating the data to humans. Recently it has been shown that nitric oxide accelerates the mito-KATP channel opening, 42 and it may be the nitric oxide effect of nicorandil that accelerates the mito-KATP channel opening.…”

Section: Discussionmentioning

confidence: 99%

Effect of Ischemic Preconditioning and Mitochondrial KATP Channel Openers on Chronic Left Ventricular Remodeling in the Ischemic-Reperfused Rat Heart.

Dairaku

Miura

Harada

et al. 2002

Circ J

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brief episode of ischemia -reperfusion reduces the size of the infarct caused by a subsequent longer ischemia -reperfusion insult. This phenomenon was first reported by Murry et al 1 and termed ischemic preconditioning (IP). The underlying mechanism of this phenomenon has been intensively investigated and one of the crucial mechanisms is the opening of the mitochondrial ATP-sensitive potassium (mito-KATP) channels. [2][3][4] In order to mimic IP, the effect of mito-KATP channel openers has been investigated and these agents result in reduction of infarct size. [5][6][7][8][9][10][11][12] However, the effect of IP and mito-KATP channel openers on chronic left ventricular (LV) remodeling has not been clarified yet. LV remodeling is a major determinant of prognosis after myocardial infarction 13 and it may be determined by the infarct size and could be modified by drugs such as angiotensin-converting enzyme inhibitors. 14 Thus, assessing LV remodeling is an important evaluation of whether or not interventions such as IP or mito-KATP channel openers are really effective. Furthermore, the reperfusion conditions, such as the no reflow phenomenon, may modify the infarct size and thus the LV remodeling in the chronic state. Therefore, the purpose of the present study was to investigate the effect of IP and mito-KATP channel openers on the extent of LV remodeling as assessed by the pressure -volume relationship, and to assess the correlation between infarct size and LV remodelCirculation Journal Vol.66, April 2002 ing during the chronic stage. MethodsAll experiments were performed in accordance with the Guide for the Care and Use of Laboratory Animals (NIH Publication No. 85-23) and were approved by the Animal Research Committee of Yamaguchi University School of Medicine. Surgical PreparationMale Sprague-Dawley rats (280-330 g) were anesthetized by intraperitoneal injection of sodium pentobarbital (60 mg/kg). Additional anesthesia was given during the experiment as required. After tracheal intubation, the rats were ventilated with a mixture of room air and 100% oxygen (respiratory rate, 65-70 breaths/min). After a thoracotomy in the fourth intercostal space, the heart was exposed and a thread was passed around the left anterior descending coronary artery (LAD) to occlude it. After 3 weeks of reperfusion, LV pressure (LVP) was measured by a 2F catheter-tip micromanometer (Model SPC-320, Millar Instruments, USA) inserted via the right carotid artery. The peak of the first derivative of LVP (+dP/dt) and the time constant of isovolumetric LVP decay (Tau) were calculated by an online data acquisition system (CODAS, DATAQ Instruments, Achron, OH, USA). The body temparature was maintained at 37±0.3°C by a heating pad. ReagentsDiazoxide (Funakoshi, Osaka, Japan) was dissolved in dimethylsulfoxide (DMSO), the final concentration of which was less than 0.1%. Nicorandil (Chugai, Tokyo, Japan) was dissolved in saline at a concentration of 1.0 J 2002; 66: 411 -415 (Received October 26, 2001; revised manuscript received December ...

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“…[32][33][34][35] In particular, mitochondrial ATP-sensitive potassium channels appear to be the end-effectors of signal transduction pathways in preconditioning. Nicorandil is believed to manifest its preconditioning effect through its pharmacological properties, being a hybrid between a nitrate and an ATP-sensitive potassium channel opener.…”

Section: Vol 43 Nomentioning

confidence: 99%

Nicorandil-Induced Preconditioning as Evidenced by Troponin T Measurements after Coronary Angioplasty in Patients with Stable Angina Pectoris.

et al. 2002

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SUMMARYNicorandil has been reported to have a preconditioning effect which suppresses the ST-segment shift or lactate production during coronary angioplasty in patients with stable angina pectoris. The present study investigated whether the preconditioning effect of nicorandil affects troponin T (TnT) levels after coronary angioplasty. Twenty-four patients with stable angina pectoris were randomized to receive a 1-minute intravenous infusion of nicorandil (100 µg/kg) or normal saline. Five minutes later they underwent three 2-minute balloon inflations 5 minutes apart. The sum of ST-segment elevation in all leads (∑ST) was determined at the end of each balloon inflation. Serum levels of TnT were measured 6 and 18 hours after the procedure, and the higher value of the two measurements was compared between the groups. ∑ST decreased progressively during the three sequential balloon inflations in both groups and was less in the nicorandil group than in the control group. The TnT level after the procedure was significantly lower in the nicorandil group than in the control group (0.05±0.05 vs 0.11±0.10 ng/mL). In conclusion, pretreatment with intravenous nicorandil suppresses TnT release after coronary angioplasty as well as ST-segment elevation during coronary angioplasty, suggesting pharmacological preconditioning by nicorandil. (Jpn Heart J 2002; 43: 443-453)

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Roles of mitochondrial ATP-sensitive K channels and PKC in anti-infarct tolerance afforded by adenosine A1receptor activation

Cited by 104 publications

References 34 publications

The Insulin Sensitizer Pioglitazone Improves the Deterioration of Ischemic Preconditioning in Type 2 Diabetes Mellitus Rats

The Insulin Sensitizer Pioglitazone Improves the Deterioration of Ischemic Preconditioning in Type 2 Diabetes Mellitus Rats

Effect of Ischemic Preconditioning and Mitochondrial KATP Channel Openers on Chronic Left Ventricular Remodeling in the Ischemic-Reperfused Rat Heart.

Nicorandil-Induced Preconditioning as Evidenced by Troponin T Measurements after Coronary Angioplasty in Patients with Stable Angina Pectoris.

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