Positive Lusitropic Effect of Quercetin on Isolated Ventricular Myocardia from Normal and Streptozotocin-Induced Diabetic Mice

Hamaguchi, Satoshi; Abe, Kohei; Komatsu, Momoka; Kainuma, Jun; Namekata, Iyuki; Tanaka, Hikaru

doi:10.1248/bpb.b21-00580

Cited by 6 publications

(4 citation statements)

References 20 publications

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“…The procedures were the same as those in our previous study. 5,6) The papillary muscles were mounted in an organ bath filled with a physiological salt solution of the following composition: 118. 5% CO 2 and maintained at 36 ± 0.5 °C.…”

Section: Methodsmentioning

confidence: 99%

Negative Inotropic Effects of Class I Antiarrhythmics on Guinea Pig Ventricular Myocardium: Correlation with L-Type Ca<sup>2+</sup> Channel Blockade

Hiiro

Hashimoto

Mizoguchi

et al. 2023

Biological & Pharmaceutical Bulletin

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The negative inotropic effects of nine Vaughan Williams class I antiarrhythmic drugs were examined in guinea pig ventricular tissue preparations. The drugs decreased the contractile force of papillary muscles with different potencies: the potency order was propafenone > aprindine > cibenzoline > flecainide > ranolazine > disopyramide > pilsicainide > mexiletine > GS-458967. The potency of drugs correlated with the reported IC 50 values to block the L-type Ca 2 channel rather than the Na channel. The effects of drugs were roughly the same when examined under a high extracellular K solution, which inactivates the Na channel. Furthermore, the attenuation of the extracellular Ca 2 -induced positive inotropy was strong with propafenone, moderate with cibenzoline, and weak with pilsicainide. These results indicate that the negative inotropic effects of class I antiarrhythmic drugs can be largely explained by their blockade of the L-type Ca 2 channel.

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Section: Methodsmentioning

confidence: 99%

Negative Inotropic Effects of Class I Antiarrhythmics on Guinea Pig Ventricular Myocardium: Correlation with L-Type Ca<sup>2+</sup> Channel Blockade

Hiiro

Hashimoto

Mizoguchi

et al. 2023

Biological & Pharmaceutical Bulletin

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“…All experiments were approved by the Ethics Committee of Toho University Faculty of Pharmaceutical Sciences (22-41-507) and performed in accordance with the Guiding Principles for the Care and Use of Laboratory Animals approved by The Japanese Pharmacological Society. The basic experimental setup and procedures were the same as those in our previous studies [ 6 , 7 , 15 , 16 , 21 , 22 , 23 , 40 , 41 , 42 , 43 ].…”

Section: Methodsmentioning

confidence: 99%

Mechanisms for the α-Adrenoceptor-Mediated Positive Inotropy in Mouse Ventricular Myocardium: Enhancing Effect of Action Potential Prolongation

Hamaguchi

Morinou

Shiseki

et al. 2023

IJMS

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Mechanisms for the α-adrenoceptor-mediated positive inotropy in neonatal mouse ventricular myocardium were studied with isolated myocardial preparations. The phenylephrine-induced positive inotropy was suppressed by prazosin, nifedipine, and chelerythrine, a protein kinase C inhibitor, but not by SEA0400, a selective Na+/Ca2+ exchanger inhibitor. Phenylephrine increased the L-type Ca2+ channel current and prolonged the action potential duration, while the voltage-dependent K+ channel current was not influenced. In the presence of cromakalim, an ATP-sensitive K+ channel opener, the phenylephrine-induced prolongation of action potential duration, as well as the positive inotropy, were smaller than in the absence of cromakalim. These results suggest that the α-adrenoceptor-mediated positive inotropy is mediated by an increase in Ca2+ influx through the L-type Ca2+ channel, and the concomitant increase in action potential duration acts as an enhancing factor.

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“…All experiments with isolated guinea pig myocardium were performed with methods substantially the same as those in our previous studies. 7,8,13,14,[16][17][18][19] This study was approved by the Animal Care and User Committee of Toho University (21-55-362).…”

Section: Methodsmentioning

confidence: 99%

Inhibitory Effect of a Late Sodium Current Blocker, NCC-3902, on the Automaticity of the Guinea Pig Pulmonary Vein Myocardium

Namekata

Hiiro

Odaka

et al. 2022

Biological & Pharmaceutical Bulletin

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The effect of blocking the persistent component of the sodium channel current (late I Na ) on the automatic activity of the isolated guinea pig pulmonary vein myocardium was examined. NCC-3902 blocked late I Na , but did not affect other major ion channel currents stably expressed in cell lines. In isolated pulmonary vein cardiomyocytes, NCC-3902 blocked the late I Na induced by a ramp depolarizing voltage clamp pulse similar to that of the pacemaker depolarization observed in the pulmonary vein myocardium. In isolated pulmonary vein tissue, NCC-3902 decreased the frequency of automatic firing of the myocardium through a reduction of the pacemaker depolarization slope. In isolated pulmonary vein cardiomyocytes, NCC-3902 significantly reduced the firing frequency of Ca 2 transients, but had no effect on Ca 2 sparks. NCC-3902 affected neither the spontaneous beating rate of the right atrium nor the contractile force of the ventricular myocardium. Selective blockers of late I Na like NCC-3902, which inhibit the automatic activity of the pulmonary vein myocardium, appear to be promising as drugs for the pharmacological treatment of atrial fibrillation.

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Positive Lusitropic Effect of Quercetin on Isolated Ventricular Myocardia from Normal and Streptozotocin-Induced Diabetic Mice

Cited by 6 publications

References 20 publications

Negative Inotropic Effects of Class I Antiarrhythmics on Guinea Pig Ventricular Myocardium: Correlation with L-Type Ca<sup>2+</sup> Channel Blockade

Negative Inotropic Effects of Class I Antiarrhythmics on Guinea Pig Ventricular Myocardium: Correlation with L-Type Ca<sup>2+</sup> Channel Blockade

Mechanisms for the α-Adrenoceptor-Mediated Positive Inotropy in Mouse Ventricular Myocardium: Enhancing Effect of Action Potential Prolongation

Inhibitory Effect of a Late Sodium Current Blocker, NCC-3902, on the Automaticity of the Guinea Pig Pulmonary Vein Myocardium

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