• Proceedings of the Ginseng society Conference
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• 1980.09a
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• pp.1-3
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• 1980

To investigate the effect of ginseng on blood pressure (B.P.) in spontaneously hypertensive rat (SHR) and essential hypertension ginseng extract was given per se daily in 58 SHR and 35 essential hypertensive patients. SHR were divided into 5 groups according to the dosage of ginseng. In essential hypertension 1,000mg of ginseng extract was given. The B.P. in SHR was measured by tail cuff method. In essential hypertension side effect and changes in various laboratory examinations were evaluated. In SHR ginseng appeared to have hypertensive effect when it is given in small amount(10mg/kg). However, when it is given 60mg/kg/day or more difinite B.P. lowering effect was observed. The hypotensive effect was dosedependant and it lasted for 37days of observation. In essential hypertension in 12 $(80\%)$ among 15 patients hypotensive effect was seen with ginseng administration along and the effect lasted for 12 weeks. In the rest of hypertensive patients it is required addition of diuretics of other antihypertensive drugs to decrease B.P., no appreciable side effect was seen. In laboratory examinations no significant changes were seen except for serum cholesterol, ${\alpha}-and\;{\beta}-lipoprotein,$ and hematocrit. There was some evidence of relationship between plasma renin activity (PRA) and ginseng in hypotensive action.

• The Korean Journal of Zoology
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• v.39 no.2
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• pp.215-222
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• 1996

In the previous studies, we have demonstrated that prorenin converting enzyme (PRECE) was identical to the epidermal grouch factor-binding protein (EGF-BP) type B, which was a member of the mouse glandular kallikrein family, To examine whether or not EGF-BP type A and C are involved in the processing of prorenin, we have cloned the CDNAS of the EGF-BP type h and C from a library of male ICR mouse submandibular gland (SMGI. And then CHO cells were transfected with the EGF-BP expression plasmids. and stable cell lines expressing a high level of the EGF-BPS precursor were obtained. The conditioned medium was then treated with trypsin, which has been knotvn to effectively convert the EGF-BP type A and C precursor to the active forms. 수ubsequentlv, the prorenin converting activity of the trypsin-treated or untreated medium was examined. PRECE converted exactly prorenin to renin, but the prorenin converting activities of EGF-BP type A and C were not detected. From these results, it seems that only type B of these EGF-BPs is involved in processing Ren 2 prorenin in mouse SMG.

• YAKHAK HOEJI
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• v.43 no.6
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• pp.843-850
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• 1999

We investigated whether endothelium-derived NO and endothelin-1 might result enhanced vasoconstriction induced by administration of norepinephrien (NE) at the early stage of one-kidney, one-clip (1K1C) renal hypertensive rats. We also studied the relation ship of renin-angiotensin system (RAS) using rat aorta in this hypothesis. L-NMMA (30$\mu$M) and L-NAME(30${\mu}M$) enhanced vasoconstriction induced by NE in thoracic aorta of control rats. However angiotensin converting enzyme (ACE) inhibitor didn't. The aorta of 1KIC rats showed a singnificantly exaggerated contractile response to NE as compared with control rats. Rub-bing the endothelium abolished this difference. Ach and SNP-induced vasorelaxation show no significant difference between 1KIC and control rats. The treatment of phosphoramidon (10${\mu}M$) and oral administration of captopril (0.05, w/v%) abolished the exaggerated contractile response to NE at early stage of 1KIC rats. These results suggest that the increase of contractile response at the early phase in 1KIC rat is partially involved in the activation of ACE.

• The Korean Journal of Physiology
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• v.24 no.2
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• pp.261-268
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• 1990

It has long been suggested that the cardiac atrium is a low pressure volume receptor controlling body fluid volume and blood pressure. Recently, the cardiac atrium has been found to contain a family of powerful peptides. To clarify the relationship between high blood pressure and the biologically active atrial peptides, experiments were done to define the characteristics of atrial natriuretic peptide secretion in the isolated perfused atria of renal hypertensive rats. Higher concentrations of plasma atrial natriuretic peptide and renin activity were observed in the two-kidney, one clip hypertensive rat compared to the normotensive rat. Atrial volume changes in response to pressure elevations were attenuated in hypertensive rats compared to normotensive rats. Incremental response to atrial volume changes in ANP secretion was accentuated in hypertensive rats. These date suggest that the accentuated atrial natriuretic peptide response to volume changes of hypertensive rats may be a physiological or pathphysiological adaptation to the high blood pressure and may be, at least in part, responsible for the elevated levels of plasma atrial natriuretic peptide observed in hypertensive rats.

• Clinical and Experimental Reproductive Medicine
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• v.48 no.3
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• pp.189-193
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• 2021

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus found in China in 2019. The disease caused by SARS-CoV-2, coronavirus disease 2019 (COVID-19), has been found to be closely related to the cells that secrete angiotensin-converting enzyme 2 (ACE2). ACE2 is involved in the renin-angiotensin system and is widely secreted in several tissues, including the testis, which has raised concerns because organs with high expression of the ACE2 receptor are susceptible to infection. Analyses have shown that in testicular cells, such as spermatogonia, seminiferous duct cells, Sertoli cells, and Leydig cells, there is a high expression level of ACE2. Therefore, SARS-CoV-2 may damage male reproductive tissues and cause infertility. Since male infertility is an important problem, scientists are evaluating whether COVID-19 may influence male infertility through the ACE2 receptor.

• Environmental Mutagens and Carcinogens
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• v.21 no.2
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• pp.72-76
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• 2001

Essential hypertension is a heterogeneously multifactorial disease in which blood pressure is harmfully high without overt cause. Both genetic and environmental factors have been implicated in its etiology. In view of the regulatory role of this peptide in the carbohydrate metabolism and renin-angiotensin system, amylin gene has been proposed to a candidate gene for essential hypertension. Therefore, we scanned the amylin gene for mutations in 133 Korean normotensives and 61 essential hypertensives by single-strand conformational polymorphism, and found a single heterozygous S20G missense mutation. However, no significant difference was observed between normotensives and essential hypertensives in the distribution of allele and genotype frequencies of this mutation at the amylin gene (P>0.05). This finding suggests that S20G missense mutation of the amylin gene are unlikely to contribute to the etiology of essential hypertension in the Korean population.

• Childhood Kidney Diseases
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• v.27 no.1
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• pp.26-33
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• 2023

Purpose: Hematuria and proteinuria have various causes and consequential outcomes in children. Immunosuppressants are needed in some children with biopsy-proven glomerulonephropathy but have many adverse effects. Since the clinical practice patterns of Korean pediatric nephrologists are diverse, we surveyed their opinions. Methods: Using a clinical vignette, the survey was emailed to all Korean Society of Pediatric Nephrology members. The questionnaires included diagnosis, examination, medications, and dietary recommendations for patients with hematuria and proteinuria. Results: A total of 32 clinicians (5.48%, 22 pediatric certificated nephrologists) responded to the survey. Most responders (87.5%) suspected immunoglobulin A nephropathy, and 68.8% replied that kidney biopsies were a diagnostic tool. Renin-angiotensin system inhibition (62.5%) or steroids (18.8%) were selected as the treatment. Salt and protein intakes were usually encouraged as dietary reference intakes (34.4% and 65.6%, respectively). Conclusions: Children with abnormal urinalysis have various causes, treatments, and prognoses. As treatments such as immunosuppressants can have many adverse effects, it is necessary to confirm an accurate diagnosis and indications of treatments before starting the treatment. Recommendations for a diet should not hinder growth.

• Journal of Ginseng Research
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• v.48 no.2
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• pp.113-121
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• 2024

Since its outbreak in late 2019, the Coronavirus disease 2019 (COVID-19) pandemic has profoundly caused global morbidity and deaths. The COVID-19 pandemic caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has major complications in cardiovascular and pulmonary system. The increased rate of mortality is due to delayed detection of certain biomarkers that are crucial in the development of disease. Furthermore, certain proteins and enzymes in cellular signaling pathways play an important role in replication of SARS-CoV-2. Most cases are mild to moderate symptoms, however severe cases of COVID-19 leads to death. Detecting the level of biomarkers such as C-reactive protein, cardiac troponin, creatine kinase, creatine kinaseMB, procalcitonin and Matrix metalloproteinases helps in early detection of the severity of disease. Similarly, through downregulating Renin-angiotensin system, interleukin, Mitogen-activated protein kinases and Phosphoinositide 3-kinases pathways, COVID-19 can be effectively controlled and mortality could be prevented. Ginseng and ginsenosides possess therapeutic potential in cardiac and pulmonary complications, there are several studies performed in which they have suppressed these biomarkers and downregulated the pathways, thereby inhibiting the further spread of disease. Supplementation with ginseng or ginsenoside could act on multiple pathways to reduce the level of biomarkers significantly and alleviate cardiac and pulmonary damage. Therefore, this review summarizes the potential of ginseng extract and ginsenosides in controlling the cardiovascular and pulmonary diseases by COVID-19.

• Korean Circulation Journal
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• v.52 no.3
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• pp.173-197
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• 2022

Treatment options for patients with heart failure (HF) with reduced ejection fraction (HFrEF) have expanded considerably over the past few decades. Whereas neurohormonal modulation remains central to the management of patients with HFrEF, other pathways have been targeted with drugs that have novel mechanisms of action. The angiotensin receptor-neprilysin inhibitors (ARNIs) which enhance levels of compensatory molecules such as the natriuretic peptides while simultaneously providing angiotensin receptor blockade have emerged as the preferred strategy for inhibiting the renin angiotensin system. Sodium glucose cotransporter 2 (SGLT2) inhibitors which were developed as hypoglycemic agents have been shown to improve outcomes in patients with HF regardless of their diabetic status. These agents along with beta blockers and mineralocorticoid receptor antagonists are the core medical therapies for patients with HFrEF. Additional approaches using ivabradine to slow heart rate in patients with sinus rhythm, the hydralazine/isosorbide dinitrate combination to unload the heart, digoxin to provide inotropic support and vericiguat to augment cyclic guanosine monophosphate production have been shown in well-designed trials to have beneficial effects in the HFrEF population and are used as adjuncts to the core therapies in selected patients. This review provides an overview of the medical management of patients with HFrEF with focus on the major developments that have taken place in the field. It offers prospective of how these drugs should be employed in clinical practice and also a glimpse into some strategies that may prove to be useful in the future.

• The Korean Journal of Physiology
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• v.19 no.1
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• pp.35-48
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• 1985

One of most frequently used anesthetic agents is barbiturate derivatives. Pentobarbital or thiopental sodium have been used most frequently in the laboratory or clinical practice. There have been reports on the renal effects of barbiturate anesthesia in human and laboartory animals. Renal effects of thiopental sodium anesthesia, however, are still controversial. One of the discrepancies may be derived from the doses used. It has been reported that subanesthetic small dose of thiopental sodium influences the renal function directly. To clarify possible central effects of very small amounts of thiopental sodium on the renal function, experiments have been done in conscious rabbits. Thiopental sodium was infused into the lateral cerebroventricle for 10 minutes. Intracerebroventricular thiopental sodium induced increased urinary volume, glomerular filtration rate and renal plasma flow by doses of $0.1{\sim}1.0\;mg/10 min/rabbit$. Filtration fractions were not changed. Sodium, chloride and potassium excretions were increased by 0.065 mg/10 min/rabbit of thiopental sodium without significant changes of renal hemodynamics. Higher doses of thiopental sodium $(0.1{\sim}1.0\;mg/10 min/rabbit)$ induced greater increases of electrolytes excretion and renal hemodynamics. Free water clearance was not changed by thiopental sodium, but the fractional excretion of free water showed a tendency of decrease. Fractional excretion of sodium was increased by doses of 0.065 to 1.0 mg of thiopental sodium . Highly significant correlation between the changes of glomerular filtration rate and the changes of sodium excretion were found in the higher doses. Plasma renin concentration (activity) was not changed by the centrally administered thiopental sodium. Intravenous thiopental sodium, 1.0 mg/rabbit, induced no changes of renal function in conscious rabbit. These data suggest that intracerebroyentricular thiopental sodium can increase urinary sodium excretion directly by inhibition of sodium reabsorption in the renal tubules and/or indirectly by increasing the renal hemodynamics.