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Takashi Ueyama - One of the best experts on this subject based on the ideXlab platform.
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amlodipine has a preventive effect on temporal left ventricular hypokinesia after Emotional Stress compared with an angiotensin ii receptor blocker
Journal of Medical Ultrasonics, 2013Co-Authors: Fuminobu Ishikura, Yuri Takano, Takashi UeyamaAbstract:We previously reported that α- and β-blockers protected against Emotional Stress-induced cardiac dysfunction, but the protective effects of other antihypertensive drugs is unknown. The purpose of this study is to evaluate the ability of a calcium channel blocker, amlodipine, to prevent temporal left ventricular hypokinesia after Emotional Stress compared with an angiotensin II receptor blocker, olmesartan medoxomil. Rats premedicated with amlodipine (0.2 mg/kg), olmesartan (0.8 mg/kg), or vehicle were restrained for 30 min (immobilization Stress: IMO) to reproduce Emotional Stress and then anesthetized to release Stress. We measured the fractional area change (FAC) using echocardiography (SONOS5500) with a s12 probe (frequency 5–12 MHz, frame rate 120 Hz) and blood pressure and heart rate at the end of IMO and every 10 for 60 min after IMO. During IMO, FAC in the amlodipine or the olmesartan group was as high as that in the vehicle group. At 20 min after IMO, FAC in the amlodipine group was significantly higher than in the other two groups (84 ± 8 vs. 60 ± 7 or 68 ± 15 %, p < 0.05). During IMO, blood pressure in the amlodipine or the olmesartan group was significantly lower than with vehicle (119 ± 6 and 110 ± 7 vs. 124 ± 5 mmHg, p < 0.05). After IMO, blood pressure in the olmesartan group was significantly lower than in the other two groups. Acute administration of amlodipine could prevent a sudden drop in cardiac function after acute Stress like IMO, but olmesartan did not. Amlodipine might have a protective effect on temporal left ventricular hypokinesia after Emotional Stress, which might not be related to decreased blood pressure.
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catecholamines and estrogen are involved in the pathogenesis of Emotional Stress induced acute heart attack
Annals of the New York Academy of Sciences, 2008Co-Authors: Takashi Ueyama, Ken Kasamatsu, Takuzo Hano, Yoshihiro Tsuruo, Fuminobu IshikuraAbstract:Emotional Stress triggers takotsubo cardiomyopathy in postmenopausal women. Clinical analysis of autonomic nervous function has revealed a transient increase of sympathetic nervous activity and decrease of vagal nervous activity. Immobilization (IMO) Stress of rats can reproduce the electrocardiographic and left ventriculographic changes that occur in takotsubo cardiomyopathy, both of which are prevented by combined blockade of alpha- and beta-adrenoceptors. Estrogen supplementation partially attenuated these cardiac changes. It also attenuated the IMO-induced increase of c-Fos immunoreactivity, or c-fos mRNA expression in the lateral septum, medial amygdaloid nucleus, paraventricular hypothalamic nucleus, dorsomedial hypothalamic nucleus, laterodorsal tegmental nucleus, and locus ceruleus; these regions contain central sympathetic neurons and neurons with immunoreactive estrogen receptors. It also downregulated c-fos mRNA expression in the adrenal gland and the heart, suggesting an increase of estrogen attenuated the Stress-induced hypothalamo-sympathoadrenal outflow from the central nervous system to the target organs. Estrogen treatment also upregulated the levels of cardioprotective substances, such as atrial natriuretic peptide and heat shock protein 70, in the heart. These data suggest that reduction of estrogen levels following menopause might be involved in the primary cause of takotsubo cardiomyopathy both by indirect action on the nervous system and by direct action on the heart.
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chronic estrogen supplementation following ovariectomy improves the Emotional Stress induced cardiovascular responses by indirect action on the nervous system and by direct action on the heart
Circulation, 2007Co-Authors: Takashi Ueyama, Fuminobu Ishikura, Ken Kasamatsu, Takuzo Hano, Akiko Matsuda, Toshihiko Asanuma, Kazuki Ueda, Masao Ichinose, Takashi Akasaka, Yoshihiro TsuruoAbstract:Background Takotsubo cardiomyopathy is triggered by Emotional or physical Stress especially in post-menopausal women. A reduction in estrogen levels following menopause might underlie the high incidence of takotsubo cardiomyopathy. Methods and Results The left ventricular contraction between ovariectomized rats (OVX) and OVX with estrogen supplementation (OVX + E) while subjected to immobilization Stress (IMO) was compared. The IMO in combination with general anesthesia impaired the left ventricular contraction in both OVX and OVX + E. Estrogen supplementation tended to improve the IMO-induced cardiac dysfunction and significantly attenuated the increase of blood pressure and heart rate. To understand the protective mechanism of estrogen, the expression of c-fos mRNA, a marker of cellular activation was compared. The mRNA expression of cardioprotective substances in the heart was also investigated. In the OVX + E, the levels of c-fos mRNA were significantly decreased in the paraventricular hypothalamic nucleus, adrenal gland and left ventricle, suggesting that an increase of estrogen attenuates the Emotional Stress-induced hypothalamo-sympatho-adrenal outflow from the central nervous system to the target organs. An expression of heat shock protein 70 and atrial natriuretic peptide was significantly augmented in the OVX + E. Conclusions These data suggest that estrogen supplementation partially prevents Emotional Stress-induced cardiovascular responses both by indirect action on the nervous system and by direct action on the heart. (Circ J 2007; 71: 565 - 573)
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Emotional Stress induced tako tsubo cardiomyopathy animal model and molecular mechanism
Annals of the New York Academy of Sciences, 2004Co-Authors: Takashi UeyamaAbstract:Emotional or physical Stress triggers Tako-tsubo cardiomyopathy in postmenopausal females, which is characterized by an elevation of the ST segment in the electrocardiogram (ECG) and left ventricular apical ballooning in the left ventriculogram (LVG). Immobilization Stress (IMO) of rats can reproduce these ECG and LVG changes, both of which are normalized by combined blockade of alpha- and beta-adrenoceptors. An increase of serum estrogen partially attenuated these cardiac changes. IMO induced a rapid activation of p44/p42 mitogen-activated protein kinase, followed by a transient upregulation of immediate early genes (IEG) in the coronary artery and myocardium. Blocking of both alpha- and beta-adrenoceptors eliminated the upregulation of IEG induced by Stress, while alpha- or beta-agonists upregulated IEG in the perfused heart. Heat shock protein 70 was induced in the aorta, coronary artery, and the myocardium. Natriuretic peptide genes (ANP and BNP) were also upregulated in the myocardium. Sequential gene expression can be considered as an adaptive response to Stress. Activation of alpha- or beta-adrenoceptors is the primary trigger of Emotional Stress-induced cardiac changes.
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estrogen attenuates the Emotional Stress induced cardiac responses in the animal model of tako tsubo ampulla cardiomyopathy
Journal of Cardiovascular Pharmacology, 2003Co-Authors: Takashi Ueyama, Ken Kasamatsu, Takuzo Hano, Katsuhiro Yamamoto, Yoshihiro Tsuruo, Ichiro NishioAbstract:Reduction of estrogen levels may underlie the high incidence of 'Tako-tsubo (Ampulla) cardiomyopathy in postmenopausal females. Ovariectomized (OVX) and estradiol-supplemented ovariectomized female rats (OVX + E) were subjected to immobilization Stress, an animal model of Tako-tsubo cardiomyopathy. In order to evaluate cardiac changes, left ventriculography and electrocardiography were performed under anesthesia (control). Next day, the conscious rats were exposed to immobilization Stress, and left ventriculography was performed (Stress). In OVX rats, percentage contraction in left ventriculography was significantly reduced in response to Stress, while it was not significantly changed in OVX + E rats. In both groups, heart rate was significantly increased in response to Stress. However, heart rate in Stress was significantly higher in OVX than in OVX + E rats. In summary, these data suggest that increase of serum estradiol levels can diminish the pathological changes in the heart induced by Emotional Stress.
Christoph A Karle - One of the best experts on this subject based on the ideXlab platform.
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adrenergic regulation of the rapid component of the cardiac delayed rectifier potassium current ikr and the underlying herg ion channel
Basic Research in Cardiology, 2004Co-Authors: Dierk Thomas, Johann Kiehn, Hugo A Katus, Christoph A KarleAbstract:Ventricular arrhythmias are often precipitated by physical or Emotional Stress, in particular in patients with ischemic heart disease or hereditary long QT syndrome. Stimulation of the sympathetic nervous system in response to exercise or Emotional Stress causes activation of cardiac α- and β-adrenoceptors. The rapid component of the delayed rectifier potassium current, IKr, and the underlying hERG potassium channel are critical for the regulation of heart rhythm. Recent experimental studies revealed that hERG/IKr currents are modulated by α- and β-adrenergic stimulation, providing a pathophysiological explanation for the increased incidence of arrhythmias during Stress. This review summarizes the current knowledge on hERG/IKr channel modulation by adrenergic activity. In addition, therapeutic approaches to future effective, more genotype-specific antiarrhythmic therapies are discussed.
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adrenergic regulation of the rapid component of the cardiac delayed rectifier potassium current i kr and the underlying herg ion channel
Basic Research in Cardiology, 2004Co-Authors: Dierk Thomas, Johann Kiehn, Hugo A Katus, Christoph A KarleAbstract:Ventricular arrhythmias are often precipitated by physical or Emotional Stress, in particular in patients with ischemic heart disease or hereditary long QT syndrome. Stimulation of the sympathetic nervous system in response to exercise or Emotional Stress causes activation of cardiac alpha- and beta-adrenoceptors. The rapid component of the delayed rectifier potassium current, I(Kr), and the underlying hERG potassium channel are critical for the regulation of heart rhythm. Recent experimental studies revealed that hERG/I(Kr) currents are modulated by alpha- and beta-adrenergic stimulation, providing a pathophysiological explanation for the increased incidence of arrhythmias during Stress. This review summarizes the current knowledge on hERG/I(Kr) channel modulation by adrenergic activity. In addition, therapeutic approaches to future effective, more genotype-specific antiarrhythmic therapies are discussed.
Dierk Thomas - One of the best experts on this subject based on the ideXlab platform.
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adrenergic regulation of the rapid component of the cardiac delayed rectifier potassium current ikr and the underlying herg ion channel
Basic Research in Cardiology, 2004Co-Authors: Dierk Thomas, Johann Kiehn, Hugo A Katus, Christoph A KarleAbstract:Ventricular arrhythmias are often precipitated by physical or Emotional Stress, in particular in patients with ischemic heart disease or hereditary long QT syndrome. Stimulation of the sympathetic nervous system in response to exercise or Emotional Stress causes activation of cardiac α- and β-adrenoceptors. The rapid component of the delayed rectifier potassium current, IKr, and the underlying hERG potassium channel are critical for the regulation of heart rhythm. Recent experimental studies revealed that hERG/IKr currents are modulated by α- and β-adrenergic stimulation, providing a pathophysiological explanation for the increased incidence of arrhythmias during Stress. This review summarizes the current knowledge on hERG/IKr channel modulation by adrenergic activity. In addition, therapeutic approaches to future effective, more genotype-specific antiarrhythmic therapies are discussed.
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adrenergic regulation of the rapid component of the cardiac delayed rectifier potassium current i kr and the underlying herg ion channel
Basic Research in Cardiology, 2004Co-Authors: Dierk Thomas, Johann Kiehn, Hugo A Katus, Christoph A KarleAbstract:Ventricular arrhythmias are often precipitated by physical or Emotional Stress, in particular in patients with ischemic heart disease or hereditary long QT syndrome. Stimulation of the sympathetic nervous system in response to exercise or Emotional Stress causes activation of cardiac alpha- and beta-adrenoceptors. The rapid component of the delayed rectifier potassium current, I(Kr), and the underlying hERG potassium channel are critical for the regulation of heart rhythm. Recent experimental studies revealed that hERG/I(Kr) currents are modulated by alpha- and beta-adrenergic stimulation, providing a pathophysiological explanation for the increased incidence of arrhythmias during Stress. This review summarizes the current knowledge on hERG/I(Kr) channel modulation by adrenergic activity. In addition, therapeutic approaches to future effective, more genotype-specific antiarrhythmic therapies are discussed.
Ichiro Nishio - One of the best experts on this subject based on the ideXlab platform.
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estrogen attenuates the Emotional Stress induced cardiac responses in the animal model of tako tsubo ampulla cardiomyopathy
Journal of Cardiovascular Pharmacology, 2003Co-Authors: Takashi Ueyama, Ken Kasamatsu, Takuzo Hano, Katsuhiro Yamamoto, Yoshihiro Tsuruo, Ichiro NishioAbstract:Reduction of estrogen levels may underlie the high incidence of 'Tako-tsubo (Ampulla) cardiomyopathy in postmenopausal females. Ovariectomized (OVX) and estradiol-supplemented ovariectomized female rats (OVX + E) were subjected to immobilization Stress, an animal model of Tako-tsubo cardiomyopathy. In order to evaluate cardiac changes, left ventriculography and electrocardiography were performed under anesthesia (control). Next day, the conscious rats were exposed to immobilization Stress, and left ventriculography was performed (Stress). In OVX rats, percentage contraction in left ventriculography was significantly reduced in response to Stress, while it was not significantly changed in OVX + E rats. In both groups, heart rate was significantly increased in response to Stress. However, heart rate in Stress was significantly higher in OVX than in OVX + E rats. In summary, these data suggest that increase of serum estradiol levels can diminish the pathological changes in the heart induced by Emotional Stress.
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molecular mechanism of Emotional Stress induced and catecholamine induced heart attack
Journal of Cardiovascular Pharmacology, 2003Co-Authors: Takashi Ueyama, Emiko Senba, Ken Kasamatsu, Takuzo Hano, Katsuhiro Yamamoto, Ichiro Nishio, Yoshihiro Tsuruo, Kenichi YoshidaAbstract:Emotional or physical Stress triggers 'tako-tsubo' cardiomyopathy or 'transient left ventricular apical ballooning', but the pathogenesis is unclear. In response to the immobilization Stress of rats, a useful model of Emotional Stress, rapid activation of p44/p42 mitogen-activated protein kinase was observed in the heart, followed by a transient upregulation of immediate early genes in the smooth muscle cells of coronary arteries, the endothelial cells and the myocardium. Heat shock protein 70 was induced in the aortic and coronary arterial smooth muscle cells and in the myocardium. Natriuretic peptide genes were also upregulated in the myocardium. Sequential gene expression can be considered as an adaptive response to Emotional Stress. Blocking of both alpha-adrenoceptors and beta-adrenoceptors eliminated the upregulation of immediate early genes induced by Stress, while alpha-agonists and beta-agonists upregulated immediate early genes in the perfused heart. Activation of alpha-adrenoceptors and beta-adrenoceptors is the primary trigger of Emotional Stress-induced molecular changes in the heart.
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Emotional Stress induces transient left ventricular hypocontraction in the rat via activation of cardiac adrenoceptors a possible animal model of tako tsubo cardiomyopathy
Circulation, 2002Co-Authors: Takashi Ueyama, Ken Kasamatsu, Takuzo Hano, Katsuhiro Yamamoto, Yoshihiro Tsuruo, Ichiro NishioAbstract:The etiology of a novel cardiac syndrome 'tako-tsubo' cardiomyopathy, otherwise known as 'transient left ventricular (LV) apical ballooning' and which mimics acute myocardial infarction, is not clear; however, Emotional or physical Stress is known to precede the attack. Left ventriculography of rats experiencing Emotional Stress induced reversible LV apical ballooning, which was normalized by pretreatment with adrenoceptor blockade. Together with results of previous studies, activation of cardiac adrenoceptors in the absence of ischemia-reperfusion is proposed as the primary cause of this syndrome.
Yoshihiro Tsuruo - One of the best experts on this subject based on the ideXlab platform.
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catecholamines and estrogen are involved in the pathogenesis of Emotional Stress induced acute heart attack
Annals of the New York Academy of Sciences, 2008Co-Authors: Takashi Ueyama, Ken Kasamatsu, Takuzo Hano, Yoshihiro Tsuruo, Fuminobu IshikuraAbstract:Emotional Stress triggers takotsubo cardiomyopathy in postmenopausal women. Clinical analysis of autonomic nervous function has revealed a transient increase of sympathetic nervous activity and decrease of vagal nervous activity. Immobilization (IMO) Stress of rats can reproduce the electrocardiographic and left ventriculographic changes that occur in takotsubo cardiomyopathy, both of which are prevented by combined blockade of alpha- and beta-adrenoceptors. Estrogen supplementation partially attenuated these cardiac changes. It also attenuated the IMO-induced increase of c-Fos immunoreactivity, or c-fos mRNA expression in the lateral septum, medial amygdaloid nucleus, paraventricular hypothalamic nucleus, dorsomedial hypothalamic nucleus, laterodorsal tegmental nucleus, and locus ceruleus; these regions contain central sympathetic neurons and neurons with immunoreactive estrogen receptors. It also downregulated c-fos mRNA expression in the adrenal gland and the heart, suggesting an increase of estrogen attenuated the Stress-induced hypothalamo-sympathoadrenal outflow from the central nervous system to the target organs. Estrogen treatment also upregulated the levels of cardioprotective substances, such as atrial natriuretic peptide and heat shock protein 70, in the heart. These data suggest that reduction of estrogen levels following menopause might be involved in the primary cause of takotsubo cardiomyopathy both by indirect action on the nervous system and by direct action on the heart.
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chronic estrogen supplementation following ovariectomy improves the Emotional Stress induced cardiovascular responses by indirect action on the nervous system and by direct action on the heart
Circulation, 2007Co-Authors: Takashi Ueyama, Fuminobu Ishikura, Ken Kasamatsu, Takuzo Hano, Akiko Matsuda, Toshihiko Asanuma, Kazuki Ueda, Masao Ichinose, Takashi Akasaka, Yoshihiro TsuruoAbstract:Background Takotsubo cardiomyopathy is triggered by Emotional or physical Stress especially in post-menopausal women. A reduction in estrogen levels following menopause might underlie the high incidence of takotsubo cardiomyopathy. Methods and Results The left ventricular contraction between ovariectomized rats (OVX) and OVX with estrogen supplementation (OVX + E) while subjected to immobilization Stress (IMO) was compared. The IMO in combination with general anesthesia impaired the left ventricular contraction in both OVX and OVX + E. Estrogen supplementation tended to improve the IMO-induced cardiac dysfunction and significantly attenuated the increase of blood pressure and heart rate. To understand the protective mechanism of estrogen, the expression of c-fos mRNA, a marker of cellular activation was compared. The mRNA expression of cardioprotective substances in the heart was also investigated. In the OVX + E, the levels of c-fos mRNA were significantly decreased in the paraventricular hypothalamic nucleus, adrenal gland and left ventricle, suggesting that an increase of estrogen attenuates the Emotional Stress-induced hypothalamo-sympatho-adrenal outflow from the central nervous system to the target organs. An expression of heat shock protein 70 and atrial natriuretic peptide was significantly augmented in the OVX + E. Conclusions These data suggest that estrogen supplementation partially prevents Emotional Stress-induced cardiovascular responses both by indirect action on the nervous system and by direct action on the heart. (Circ J 2007; 71: 565 - 573)
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estrogen attenuates the Emotional Stress induced cardiac responses in the animal model of tako tsubo ampulla cardiomyopathy
Journal of Cardiovascular Pharmacology, 2003Co-Authors: Takashi Ueyama, Ken Kasamatsu, Takuzo Hano, Katsuhiro Yamamoto, Yoshihiro Tsuruo, Ichiro NishioAbstract:Reduction of estrogen levels may underlie the high incidence of 'Tako-tsubo (Ampulla) cardiomyopathy in postmenopausal females. Ovariectomized (OVX) and estradiol-supplemented ovariectomized female rats (OVX + E) were subjected to immobilization Stress, an animal model of Tako-tsubo cardiomyopathy. In order to evaluate cardiac changes, left ventriculography and electrocardiography were performed under anesthesia (control). Next day, the conscious rats were exposed to immobilization Stress, and left ventriculography was performed (Stress). In OVX rats, percentage contraction in left ventriculography was significantly reduced in response to Stress, while it was not significantly changed in OVX + E rats. In both groups, heart rate was significantly increased in response to Stress. However, heart rate in Stress was significantly higher in OVX than in OVX + E rats. In summary, these data suggest that increase of serum estradiol levels can diminish the pathological changes in the heart induced by Emotional Stress.
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molecular mechanism of Emotional Stress induced and catecholamine induced heart attack
Journal of Cardiovascular Pharmacology, 2003Co-Authors: Takashi Ueyama, Emiko Senba, Ken Kasamatsu, Takuzo Hano, Katsuhiro Yamamoto, Ichiro Nishio, Yoshihiro Tsuruo, Kenichi YoshidaAbstract:Emotional or physical Stress triggers 'tako-tsubo' cardiomyopathy or 'transient left ventricular apical ballooning', but the pathogenesis is unclear. In response to the immobilization Stress of rats, a useful model of Emotional Stress, rapid activation of p44/p42 mitogen-activated protein kinase was observed in the heart, followed by a transient upregulation of immediate early genes in the smooth muscle cells of coronary arteries, the endothelial cells and the myocardium. Heat shock protein 70 was induced in the aortic and coronary arterial smooth muscle cells and in the myocardium. Natriuretic peptide genes were also upregulated in the myocardium. Sequential gene expression can be considered as an adaptive response to Emotional Stress. Blocking of both alpha-adrenoceptors and beta-adrenoceptors eliminated the upregulation of immediate early genes induced by Stress, while alpha-agonists and beta-agonists upregulated immediate early genes in the perfused heart. Activation of alpha-adrenoceptors and beta-adrenoceptors is the primary trigger of Emotional Stress-induced molecular changes in the heart.
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Emotional Stress induces transient left ventricular hypocontraction in the rat via activation of cardiac adrenoceptors a possible animal model of tako tsubo cardiomyopathy
Circulation, 2002Co-Authors: Takashi Ueyama, Ken Kasamatsu, Takuzo Hano, Katsuhiro Yamamoto, Yoshihiro Tsuruo, Ichiro NishioAbstract:The etiology of a novel cardiac syndrome 'tako-tsubo' cardiomyopathy, otherwise known as 'transient left ventricular (LV) apical ballooning' and which mimics acute myocardial infarction, is not clear; however, Emotional or physical Stress is known to precede the attack. Left ventriculography of rats experiencing Emotional Stress induced reversible LV apical ballooning, which was normalized by pretreatment with adrenoceptor blockade. Together with results of previous studies, activation of cardiac adrenoceptors in the absence of ischemia-reperfusion is proposed as the primary cause of this syndrome.
