• The Korean Journal of Physiology and Pharmacology
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• v.6 no.2
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• pp.121-125
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• 2002

The pathophysiological implications of aldosterone and adrenomedullin in the cardiac ventricular hypertrophy were examined. Male Sprague-Dawley rats were treated with deoxycorticosterone acetate (DOCA)-salt and monocrotaline (MCT) to selectively elicit left and right ventricular (LV, RV) hypertrophy, respectively. The mRNA expression of aldosterone synthase and adrenomedullin in LV and RV was determined by reverse transcription-polymerase chain reaction. The expression of aldosterone synthase and adrenomedullin was increased in LV, while not altered significantly in RV of DOCA-salt-treated rats. On the contrary, the expression was not significantly altered in LV, but increased in RV of MCT-treated rats. The enhanced expression of aldosterone synthase may be causally related with the development of ventricular hypertrophy, and the increased expression of adrenomedullin may act as a counter-regulatory mechanism.

• Journal of Life Science
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• v.17 no.12
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• pp.1717-1722
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• 2007

In the present study, all of the treadmill exercise-trained SHR expressed clear adaptive changes such as reduced resting heart rate and blood pressures, LPOA, homocysteine Therefore, treadmill exercise was sufficient to induce physiological adaptation in the SHR. Endurance training is known to induce physiological cardiac hypertrophy, while hypertension induces patho logical cardiac hypertrophy that increases cardiomyocyte apoptosis. The pathological adaptation to pressure overload has also been associated with a further increase in the expression of several marker genes including cardiomyocyte ET-1 in the SHR, but not in the exercise-trained SHR. Additionally, there is an increase in the endothelial nitricoxide synthases (eNOS) protein expression of soleus, gastrocnemius, and extensor digitorum longus muscle in the exercise-trained SHR but not in the SHR in the present study. Thus, compared to pathological adaptation to pressure overload, physiological adaptation to exercise training is associated with distinct alterations in cardiac and molecular phenotypes. based on these results, exercise training improves hypertension by cardiovascular regulating genes and hemodynamic parameters.

• BMB Reports
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• v.52 no.10
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• pp.595-600
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• 2019

Cardiac fibrosis is a common feature in chronic hypertension patients with advanced heart failure, and endothelial-to-mesenchymal transition (EndMT) is known to promote Angiotensin II (Ang II)-mediated cardiac fibrosis. Previous studies have suggested a potential role for the transcription factor, ETS-1, in Ang II-mediated cardiac remodeling, however the mechanism are not well defined. In this study, we found that mice with endothelial Ets-1 deletion showed reduced cardiac fibrosis and hypertrophy following Ang II infusion. The reduced cardiac fibrosis was accompanied by decreased expression of fibrotic matrix genes, reduced EndMT with decreased Snail, Slug, Twist, and ZEB1 expression, as well as reduced cardiac hypertrophy and expression of hypertrophy-associated genes was observed. In vitro studies using cultured H5V cells further confirmed that ETS-1 knockdown inhibited $TGF-{\beta}1$-induced EndMT. This study revealed that deletion of endothelial Ets-1 attenuated Ang II-induced cardiac fibrosis via inhibition of EndMT, indicating an important ETS-1 function in mediating EndMT. Inhibition of ETS-1 could be a potential therapeutic strategy for treatment of heart failure secondary to chronic hypertension.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.1
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• pp.33-40
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• 2001

The aim of present study was to define the cellular mechanisms underlying changes in delayed rectifier $K^+\;(K_{DR})$ channel function in isoproterenol-induced hypertrophy. It has been proposed that $K_{DR}$ channels play a role in regulation of vascular tone by limiting membrane depolarization in arterial smooth muscle cells. The alterations of the properties of coronary $K_{DR}$ channels have not been studied as a possible mechanism for impaired coronary reserve in cardiac hypertrophy. The present study was carried out to compare the properties of coronary $K_{DR}$ channels in normal and hypertrophied hearts. These channels were measured from rabbit coronary smooth muscle cells using a patch clamp technique. The main findings of the study are as follows: (1) the $K_{DR}$ current density was decreased without changes of the channel kinetics in isoproterenol-induced hypertrophy; (2) the sensitivity of coronary $K_{DR}$ channels to 4-AP was increased in isoproterenol-induced hypertrophy. From the above results, we suggest for the first time that the alteration of $K_{DR}$ channels may limit vasodilating responses to several stimuli and may be involved in impaired coronary reserve in isoproterenol-induced hypertrophy.

• The Journal of Internal Korean Medicine
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• v.22 no.3
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• pp.463-469
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• 2001

Valvular heart disease is one of the main current of cardiac problems and has many problems must be solved by sequelae and complications, etc. Rheumatic Mitral Stenosis is mainly attacked by rheumatic fever and developed by process of treatment of mitral valve or formation of trace. The purpose of this study is to examine the efficacy of oriental treatment for Cerebral Infarction with Rheumatic Mitral Stenosis. At the time of visiting ER, he was shown the symptoms of dull mentality, Rt. hemiplegia, global aphasia, dysphagia, chest discomfort, insomnia, dyspnea, etc, It showed that Atrial fibrillation in EKG monitoring, Atrial fibrillation, Rheumatic Mitral Stenosis, Ejection-Fraction slope 60% in Cardiac echography, Lt. atrial hypertrophy, Rt. atrial hypertrophy, Rt. ventricular hypertrophy with pulmonary congestion in chest X-ray. From the view of oriental diagnostic criteria. We classified the patient's clinical conditions and treated accordingly. As a result of treatment, symptoms were markedly improved and he was discharged. Further elaboration of oriental diagnostic classification could possibly lead to the fundamental treatment.

• BMB Reports
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• v.47 no.4
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• pp.192-196
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• 2014

RNA polymerase II carboxyl-terminal domain (pol II CTD) phosphatases are a newly emerging family of phosphatases that are members of DXDX (T/V). The subfamily includes Small CTD phosphatases, like SCP1, SCP2, SCP3, TIMM50, HSPC129 and UBLCP. Extensive study of SCP1 has elicited the diversified roles of the small C terminal domain phosphatase. The SCP1 plays a vital role in various biological activities, like neuronal gene silencing and preferential Ser5 dephosphorylation, acts as a cardiac hypertrophy inducer with the help of its intronic miRNAs, and has shown a key role in cell cycle regulation. This short review offers an explanation of the mechanism of action of small CTD phosphatases, in different biological activities and metabolic processes.

• Journal of Ginseng Research
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• v.33 no.4
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• pp.260-267
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• 2009

Recent studies have shown that Panax ginseng has a variety of beneficial effects on the cardiovascular system. Homocysteine (Hcy), which is derived from methionine, has been closely associated with the increased risk of cardiovascular diseases. In the present study, whether the in-vivo long-term co-administration of ginseng total saponins (GTS), active ingredients of Panax ginseng, with L-methionine (Met) inhibits methionine-induced hyperhomocysteine (HHcy) and H-Hcy-induced cardiovascular dysfunctions was investigated, and it was found that the plasma Hcy level, which was measured after 30 and 60 days, in the GTS+Met co-administration group was more significantly reduced than in the Metalone-treatment group. The left-ventricle (LV) wall thickness of the heart was likewise examined in each treatment group, and it was found that the co-administration of GTS with Met significantly reduced the Met-induced LV wall thickness. The results of the study indicate that the in-vivo long-term co-administration of GTS with Met not only inhibited H-Hcy induced by long-term Met-alone administration but also attenuated the H-Hcy-induced cardiovascular dysfunctions in rats.

• Journal of Chest Surgery
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• v.19 no.1
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• pp.1-11
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• 1986

Using an experimental model of pulmonary hypertension, the effects of anticonstrictive drugs on the development of pulmonary vascular remodeling and right ventricular hypertrophy were studied. Male Sprague-Dawley rats weighing 200~250 gm were used. For the experimental model of pulmonary hypertension, a group of animal was given by a subcutaneous injection of monocrotaline on a dose of 20mg, 40mg, or 60mg per kg of body weight. After 4 weeks of injection, all animals were sacrificed. Another group of animal was given by a subcutaneous injection of monocrotaline in a dose of 40 mg per kg of body weight. The animals were sacrificed, in which they were kept alive for 1, 2, 3 and 4 weeks, respectively. For the effects of anticonstrictive drugs on the development of pulmonary vascular remodeling and right ventricular hypertrophy, the animals treated with monocrotaline were given daily by an intraperitoneal injection of phenoxybenzamine in a dose of 1.3mg/kg of body weight, and were given propranolol via their drinking water at a concentration of 400mg/liter. The animals were sacrificed after 4 weeks of administration. The hearts and lungs were examined histopathologically and morphometrically. The results obtained were summarized as follows: 1. The rats treated with monocrotaline showed an interstitial pneumonitis, medial thickening of the pulmonary small arteries and hypertrophy of the right ventricular wall. 2. The medial thickening of the pulmonary arteries in rats treated with monocrotaline was due to muscular hypertrophy and hyperplasia, and the right ventricular hypertrophy was due to hypertrophy of cardiac muscles. Both medial thickening of the pulmonary arteries and hypertrophy of right ventricular wall were more marked with time and with dose. 3. The daily intraperitoneal injection of phenoxybenzamine suppressed significantly the percentage medial thickness of pulmonary small arteries and the index of right ventricular hypertrophy in rats given a single subcutaneous injection of monocrotaline, but propranolol has shown no protective effect on the development of medial thickening of pulmonary arteries and right ventricular hypertrophy in treated with monocrotaline. The results described above suggested that monocrotaline is an alkaloid selectively inducing pulmonary hypertension and that a-adrenergic receptor is responsible for the pathogenesis of monocrotaline induced pulmonary hypertension in rat.

• Korean Journal of Acupuncture
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• v.22 no.1
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• pp.75-84
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• 2005

Objectives : Acupuncture has been used as treatment of disease in the korean medicine. In this study, it was investigated that effects of reduction of acupuncture techniques of five evolutive phase for appling excess in the heart, kidney on cardiovascular system as blood pressure and renin and atrial natriuretic peptide (ANP) in plasma, cardiac hypertrophy. Materials and methods : The experiments were performed on Sprague Dawley rats, 2K1C hypertension model was prepared by constricting the left renal artery with a sliver clip. Animals were then divided into seven groups, 2K1C induced and no treated group (Control), acupuncture on SP3 HT7(AC-1), LR1 KI1 (AC-2), SP3 HT7 LR1 KI1 (AC-3). The treatments were performed once a day for 10 days in rats. Results : The results are that the blood pressure was significantly decreased at 15days in AC-1 group. The cardiac hypertrophy was significantly decrease in AC-3 group. The activity of plasma ANP was increased in all groups without AC-1 group and the that of plasma Rein was decrease in AC-1, AC-2 groups than control group. Conclusions : These results suggest that acupuncture at SP3 HT7 and SP3 HT7 LR1 KI1 can be used as a therapy for controlling renal hypertension induced by 2K1C in the rats.

• Proceedings of the Korean Biophysical Society Conference
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• 2002.06b
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• pp.20-21
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• 2002

The inflow of Ca$\^$2＋/ through voltage-activated T-type calcium channels (T-channels) regulates a variety of cellular functions including neuronal excitability, cardiac pacemaker activity, hormone secretion, smooth muscle contraction, and fertilization. Not only are T-channels enormously important for the normal operation of cells, they also playa critical role in pathophysiological conditions such as cardiac hypertrophy and absence epilepsy.(omitted)