• Title, Summary, Keyword: angiotensin II

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Diuretic Action of Angiotensin II in Dog (Angiotensin Ⅱ의 이뇨작용(利尿作用))

  • Ko, Suk-Tai;Lee, Min-Jae;Hur, Young-Keun
    • YAKHAK HOEJI
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    • v.33 no.3
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    • pp.183-190
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    • 1989
  • Angiotensin II, adminstered (infused or injected) intravenously, elicited the antidiuretic action with the decreased parameters of renal function at a small dose ($0.01\;{\mu}g/kg/min$), whereas, at a large dose (0.03, $0.1\;{\mu}g/kg/min$ and $5.0\;{\mu}g/kg$), it produced the diuretic action accompanied the increased amounts of sodium and potassium excreted in urine ($E_{Na}\;and\;R_K$). At this time, glomerular filtration rates (GFR) were weakened slightly and renal plasma flows (RPF) were reduced markedly, and then filtration fractions (FF) were increased. Angiotensin II, infused into a renal artery, exhibited antidiuretic action at a small dose ($0.003\;{\mu}g/kg/min$), and diuretic action at a large dose ($0.01\;{\mu}g/kg/min$), only in infused (experimental) kidney. The mechanism of the action was similar to the cases of the intravenous angiotensin II. The above results suggest that angiotensin II of a large dose produced diuretic action due to mechanism inhibiting reabsorption of electrolytes in renal tubules, mainly in proximal tubule in dog.

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Activation of the renin-angiotensin system in high fructose-induced metabolic syndrome

  • Kim, Mina;Do, Ga Young;Kim, Inkyeom
    • The Korean Journal of Physiology and Pharmacology
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    • v.24 no.4
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    • pp.319-328
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    • 2020
  • High fructose intake induces hyperglycemia and hypertension. However, the mechanism by which fructose induces metabolic syndrome is largely unknown. We hypothesized that high fructose intake induces activation of the renin-angiotensin system (RAS), resulting in hypertension and metabolic syndrome. We provided 11-week-old Sprague-Dawley rats with drinking water, with or without 20% fructose, for two weeks. We measured serum renin, angiotensin II (Ang II), and aldosterone (Aldo) using ELISA kits. The expression of RAS genes was determined by quantitative reverse transcription polymerase chain reaction. High fructose intake increased body weight and water retention, regardless of food intake or urine volume. After two weeks, fructose intake induced glucose intolerance and hypertension. High fructose intake increased serum renin, Ang II, triglyceride, and cholesterol levels, but not Aldo levels. High fructose intake increased the expression of angiotensinogen in the liver; angiotensin-converting enzyme in the lungs; and renin, angiotensin II type 1a receptor (AT1aR), and angiotensin II type 1b receptor (AT1bR) in the kidneys. However, expression of AT1aR and AT1bR in the adrenal glands did not increase in rats given fructose. Taken together, these results indicate that high fructose intake induces activation of RAS, resulting in hypertension and metabolic syndrome.

멸치 가공선 자숙액 pepsin 가수분해물의 angiotensin 전환효소 저해작용

  • 지청일;이지혜;박덕천;구연숙;박재홍;박영호;김인수;김선봉
    • Proceedings of the Korean Society of Fisheries Technology Conference
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    • pp.171-172
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    • 2001
  • 체내에 널리 분포되어 있는 angiotensin 전환효소(angiotensin converting enzyme, ACE ; peptidyldipeptide hydrolase, EC 3.4.15.1)는 angiotensinogen이 renin의 특이적 분해를 받아서 생성된 불활성형인 angiotensin I의 말단 dipeptide(His-Leu)를 절단하여 octapeptide인 활성형의 angiotensin II로 전환시키며, 이렇게 생성된 angiotensin II는 직접적으로 혈압상승 작용을 하거나 adrenal로부터 sediumretaining steroid hormone인 aldosterone의 유리를 촉진시켜 체내 나트륨을 저류시킨다. (중략)

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Tissue-Specific Regulation of Angiotensinogen and Angiotensin II Receptor Gene Expression in Deoxycorticosterone Acetate-Salt Hypertensive Rats

  • Lee, Jong-Un;An, Mi-Ra
    • The Korean Journal of Physiology and Pharmacology
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    • v.3 no.3
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    • pp.315-320
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    • 1999
  • Molecular regulation of the renin-angiotensin system (RAS) was investigated in deoxycorticosterone acetate (DOCA)-salt hypertension. The expression of renin, angiotensinogen and angiotensin II receptor genes in the kidney and liver was determined by Northern blot analysis in rats which were made DOCA-salt hypertensive over the period of 2 or 4 weeks. Along with the hypertension, renin mRNA was decreased in the remnant kidney. The expression of angiotensinogen gene was not significantly altered in the kidney, but was significantly decreased in the liver. The expression of angiotensin II receptor gene was increased in the kidney, while it remained unaltered in the liver. The duration of hypertension did not affect the altered gene expression. It is suggested that the components of RAS are transcriptionally regulated in DOCA-salt hypertension in a tissue-specific manner.

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The Effects of Isolated Soyprotein and Salt Restriction on Serum Lipid and Kidney Function of Streptozotocin-Induced Diabetic Rats (분리 대두단백질 섭취와 염분 제한이 Streptozotocin으로 유도된 당뇨 횐쥐의 혈청 지질 수준 및 신장기능에 미치는 영향)

  • 정수현;박양자
    • Journal of the East Asian Society of Dietary Life
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    • v.11 no.5
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    • pp.368-378
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    • 2001
  • This study was performed to investigate the effects of isolated soyprotein and salt (NaCl) restriction on the serum lipid and the kidney functions of streptozotocin-induced diabetic rats. Sprague-Dawley males of normal and streptozotocin-induced diabetic rats were raised for 6 weeds divided into 4 groups each according to protein sources and salt levels. The sources of protein were isolated soyprotein and casein. Salt levels tested were 0.1% (normal) and 0.01% (low). The results are summarized as fellows: kidney weight, blood glucose, hemoglobinAlc, GFR and urinary protein of diabetic groups were higher than those of normal groups. Isolated soyprotein lowered total lipids, triglycerides, and total cholesterol in serum and plasma angiotensin II concentration as well as alleviated kidney enlargement and GFR in diabetic rats. Salt restriction didn\\`t affect serum lipid level but decreased GFR and increased angiotensin If concentration. In conclusion, isolated soyprotein decreased serum lipids, plasma angiotensin II concentration, sidney enlargement and GFR, while salt restriction increased plasma angiotensin II concentration. The results suggest that isolated soyprotein and salt restriction seem to cause different effects on plasma angiotensin II concentration and that isolated soyprotein might be of value in the prevention of diabetic artherosclerosis and diabetic hypertension.

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Influence of SKP 450, a $K^+$ Channel Opener, on the Pressor Actions Induced by Norepinephrine, Angiotensin II and Carotid Artery Occlusion in Rats (Norepinephrine, Angiotensin II 및 경동맥 폐쇄에 의한 혈압 상승작용에 대한 $K^+$ Channel 개방제인 SKP 450의 영향)

  • 고석태
    • Biomolecules & Therapeutics
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    • v.9 no.2
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    • pp.96-103
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    • 2001
  • These studies were investigated about influence of SKP 450, a $K^{+}$ channel opener, on the pressor actions induced by norepinephrine, angiotensin II and carotid artery occlusion in rats. Before these studies, effect of SKP 450 itself on blood pressure was examinated. SKP 450 produced the depressor action in proportionaly to dose of 0.3, 1.0 and 3.0 $\mu$g/kg given intravenously and this depressor action was weakened by pretreatment of glibenclamide, a $K^{+}$ channel blocker. The pressor action induced by norepinephrine, an alpha-adrenergic agonist, was blocked 1 hr after administation of SKP 450 in a dose of 3.0 $\mu\textrm{g}$/kg, i.v. and directly after in a dose of 6.0 $\mu\textrm{g}$/kg, i.v.. The pressor action induced by angiotensin II was blocked immediatly after treatment of SKP 450 in a dose of 3.0 $\mu\textrm{g}$/kg, i.v.. The pressor action caused by carotid artery occlusion was not affected by SKP 450 of 3.0 $\mu\textrm{g}$/kg, i.v., whereas markedly blocked by SKP 450 of 6.0 $\mu\textrm{g}$/㎦, i.v.. The potentiated-pressor actions of norepinephrine and angiotensin II by pretreatment of chlorisondamine, a autonomic ganglionic blocking agent, were also blocked by administration of SKP 450 in a dose of 6.0 $\mu\textrm{g}$/kg, i.v.. The weakened-pressor action of carotid artery occlusion by pretreatment of chlorisondamine was more weakened by SKP 450 6.0 $\mu\textrm{g}$/kg, i.v.. The results suggest that hyperpolarization formed through $K^{+}$ channel opening in cell membrane inhibits the pressor action induced norepinephrine ; angiotensin II ; and carotid artery occlusion.usion.

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Losartan Modifies Nitric Oxide-related Vasorelaxation in Isolated Aorta of Spontaneously Hypertensive Rat (선천성 고혈압흰쥐 적출대동맥에서 Nitric Oxide와 관련된 이완 반응에 Losartan이 미치는 영향)

  • Park, Bong-Gee;Han, Hyung-Soo;Kim, Choong-Young
    • The Korean Journal of Pharmacology
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    • v.30 no.3
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    • pp.337-342
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    • 1994
  • It is well known that angiotensin converting enzyme inhibitors(ACEIs) increase endothelium-dependent relaxation in aortic strips of spontaneously hypertensive rats(SHR) and this increase in relaxation may be due to altered endothelial nitric oxide breakdown. But there are few studies on the effect of the angiotensin II receptor blocker on the nitric oxide-mediated relaxation. So we attempted to investigate the effect of angiotensin II receptor blocker on the nitric oxide-dependent relaxation in isolated aorta of SHR. Two week-treatment of losartan (30 mg/kg/day) increased the acetylcholine$(10^{-9}\;to\;10^{-5}\;M)$-and histamine$(10^{-8}\;to\;10^{-4}\;M)$-induced relaxation in endothelium intact strips but 90 minutes-treatment of losartan $(10^{-4}\;M)$ showed no increase in relaxation. The phenylephrine $(10^{-7}\;M)$-induced contraction, repeated every 2 hours, was diminished gradually following lipopolysaccharide (LPS)-treatment $(100\;{\mu}g/ml)$ but there was no significant difference in enalapril- and losartan-treated group compared with control group. These results suggest that activity of the endothelial constitutive NO synthase may be changed by chronic treatment of angiotensin II receptor blockers and ACEIs but angiotensin II antagonist and ACEI have no effect on the inducible NO synthase activity in the isolated aorta of SHR

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Comparative effects of angiotensin II and angiotensin-(4-8) on blood pressure and ANP secretion in rats

  • Phuong, Hoang Thi Ai;Yu, Lamei;Park, Byung Mun;Kim, Suhn Hee
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.6
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    • pp.667-674
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    • 2017
  • Angiotensin II (Ang II) is metabolized from N-terminal by aminopeptidases and from C-terminal by Ang converting enzyme (ACE) to generate several truncated angiotensin peptides (Angs). The truncated Angs have different biological effects but it remains unknown whether Ang-(4-8) is an active peptide. The present study was to investigate the effects of Ang-(4-8) on hemodynamics and atrial natriuretic peptide (ANP) secretion using isolated beating rat atria. Atrial stretch caused increases in atrial contractility by 60% and in ANP secretion by 70%. Ang-(4-8) (0.01, 0.1, and $1{\mu}M$) suppressed high stretch-induced ANP secretion in a dose-dependent manner. Ang-(4-8) ($0.1{\mu}M$)-induced suppression of ANP secretion was attenuated by the pretreatment with an antagonist of Ang type 1 receptor ($AT_1R$) but not by an antagonist of $AT_2R$ or $AT_4R$. Ang-(4-8)-induced suppression of ANP secretion was attenuated by the pretreatment with inhibitor of phospholipase (PLC), inositol triphosphate ($IP_3$) receptor, or nonspecific protein kinase C (PKC). The potency of Ang-(4-8) to inhibit ANP secretion was similar to Ang II. However, Ang-(4-8) $10{\mu}M$ caused an increased mean arterial pressure which was similar to that by 1 nM Ang II. Therefore, we suggest that Ang-(4-8) suppresses high stretch-induced ANP secretion through the $AT_1R$ and $PLC/IP_3/PKC$ pathway. Ang-(4-8) is a biologically active peptide which functions as an inhibition mechanism of ANP secretion and an increment of blood pressure.

The Therapeutic Effect of Angiotensin II Receptor Antagonist in Idiopathic Pulmonary Fibrosis (특발성 폐섬유화증 환자의 치료에서 Angiotensin II Receptor Antagonist의 치료효과)

  • Woo, Duck Soo;Seol, Won Jong;Kyung, Sun Young;Lim, Young Hee;An, Chang Hyeok;Park, Jeong Woong;Jeong, Sung Hwan;Lee, Jae Woong
    • Tuberculosis and Respiratory Diseases
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    • v.55 no.5
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    • pp.478-487
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    • 2003
  • Background : There have been several studies showing that the angiotensin II and angiotensin converting enzyme(ACE) contributes to the apoptosis of alveolar epithelial cells in idiopathic interstitial pneumonia and the activation of fibroblasts during the process of pulmonary fibrosis. These results suggest that the pulmonary fibrosis can be inhibited by the angiotensin II receptor antagonist(AGIIRA). This study was performed to identify the therapeutic effect of AGIIRA in idiopathic pulmonary fibrosis(IPF). Method : Thirteen patients with IPF, who were diagnosed with an open lung biopsy(6 patients) and furfilling the ATS criteria(7 patients) between March 1999 and October 2001 at the Gachon medical center, were enrolled in this study. Of these patients, eight patients were treated with a regimen including AGIIRA(AT group), and five were treated without AGIIRA(NT group). The pulmonary function tests and dyspnea(ATS scale) were measured at diagnosis and 1 year after treatment. All the data was collected to analyze the therapeutic effect of AGIIRA on the patients with IPF. Results : The AT group contained 8 patients(M:F=4:4) and the NT group contained 5 patients(M:F=3:2). There was no significant difference in the serum angiotensin II level between the two groups($202.5{\pm}58.5$ vs $163.7{\pm}47.3pg/ml$, p>0.05). The AT group showed an upward trend in TLC(+3%), FVC(+4%), FEV1(+3%) and DLco(+2%) compared to the NT group(TLC(-14%), FVC(-3%), FEV1(-4%) except for DLco(+5%)). The dyspnea score in the AT group improved significantly but not in the NT group. Conclusion : These results suggest that the angiotensin II receptor antagonist may have an effect on stabilizing IPF.