• Title/Summary/Keyword: ANP

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Regulatory Role of Nitric Oxide on Atrial Natriuretic Peptide System in Normotensive and Hypertensive Rats

  • Choi, Eun-Hah;Kim, Mi-Won;Lee, Jong-Un
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.1
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    • pp.79-82
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    • 1997
  • The present study was aimed to explore an interaction between endothelium-derived nitric oxide (NO) and atrial natriuretic peptide (ANP) systems in normotensive and hypertensive states. Rats were made two-kidney, one clip (2K1C) hypertensive and supplemented with either $N^G-nitro-L-arginine$ methyl ester (L-NAME, 5 mg/100 ml drinking water) or L-arginine hydrochloride (400 mg/100 ml drinking water). One group supplied with normal tap water served as control. Sham-clipped rats were also divided into the L-NAME, L-arginine, and control groups. The plasma levels and atrial contents of ANP were determined at day 28 following clipping the renal artery. In 2K1C rats, the plasma level of ANP was higher and the atrial content was lower than in the sham-clipped control. L-Arginine increased the atrial content of ANP in association with a decreased plasma ANP, whereas L-NAME significantly affected neither parameter. The increase of blood pressure in 2K1C rats was not affected by L-arginine or L-NAME. In sham-clipped rats, the plasma level of ANP was significantly increased by L-NAME along with an increase in blood pressure. On the contrary, L-arginine did not affect the blood pressure or plasma ANP. The atrial content of ANP was significantly altered neither by L-arginine nor by L-NAME. These results suggest that NO plays a tonic inhibitory role on the ANP release with concomitant increases of the atrial tissue content. In addition, hypertension is suggested to modify the release and tissue storage of ANP.

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Effect of Atrial Natriuretic Peptide on the Proliferation and Activity of Osteoblastic Cells

  • Lee, Jong-Ryeul;Ko, Seon-Yle;Kim, Jung-Keun;Kim, Se-Won
    • The Korean Journal of Physiology and Pharmacology
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    • v.4 no.4
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    • pp.283-289
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    • 2000
  • Natriuretic peptides comprise a family of three structurally related peptides; atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). The present study was performed to investigate the effect of ANP on the proliferation and activity of ROS17/2.8 and HOS cells which are well-characterized osteoblastic cell lines. ANP dose-dependently decreased the number of ROS17/2.8 and HOS cells after 48-hour treatment. ANP generally increased the alkaline phosphatase activity of ROS17/2.8 and HOS cells after 48 hr treatment, regardless of the fact that basal activity of alkaline phosphatase was much lower in HOS cells compared to that of ROS17/1.8 cells. ANP increased the NBT reduction by ROS17/2.8 and HOS cells. ANP showed the variable but no significant effect on the nitric oxide production by ROS17/2.8 and HOS cells. ROS17/2.8 and HOS cells produced and secreted gelatinase into culture medium, and this enzyme was thought to be the gelatinase A type with the molecular weight determination. The gelatinase activity produced by ROS17/2.8 cells was increased by the treatment of ANP. However, the enzyme activity was not affected by ANP treatment in the HOS cell culture. In summary, ANP decreased the proliferation and increased the alkaline phosphatase activity and NBT reduction of osteoblasts. These results indicate that ANP is one of the important regulators of bone metabolism.

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Novel Antihypertension Mechanism of 𝛽-Glucan by Corin and ANP-Mediated Natriuresis in Mice

  • Lee, Sun Jung;Lee, Dong Hee;Kim, Ha Won
    • Mycobiology
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    • v.48 no.5
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    • pp.399-409
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    • 2020
  • Many of the 𝛽-glucans are known to have antihypertensive activities, but, except for angiotensin-converting enzyme II inhibition, the underlying mechanisms remain unclear. Corin is an atrial natriuretic peptide (ANP)-converting enzyme. Activated corin cleaves pro-ANP to ANP, which regulates water-sodium balance and lowers blood pressure. Here, we reported a novel antihypertensive mechanism of 𝛽-glucans, involved with corin and ANP in mice. We showed that multiple oral administrations of 𝛽-glucan induced the expression of corin and ANP, and also increased natriuresis in mice. Microarray analysis showed that corin gene expression was only upregulated in mice liver by multiple, not single, oral administrations of the 𝛽-glucan fraction of Phellinus baumii (BGF). Corin was induced in liver and kidney tissues by the 𝛽-glucans from zymosan and barley, as well as by BGF. In addition to P. baumii, 𝛽-glucans from two other mushrooms, Phellinus linteus and Ganoderma lucidum, also induced corin mRNA expression in mouse liver. ELISA immunoassays showed that ANP production was increased in liver tissue by all the 𝛽-glucans tested, but not in the heart and kidney. Urinary sodium excretion was significantly increased by treatment with 𝛽-glucans in the order of BGF, zymosan, and barley, both in 1% normal and 10% high-sodium diets. In conclusion, we found that the oral administration of 𝛽-glucans could induce corin expression, ANP production, and sodium excretion in mice. Our findings will be helpful for investigations of 𝛽-glucans in corin and ANP-related fields, including blood pressure, salt-water balance, and circulation.

Effects of Atrial Natriuretic Peptide on Renal and Hormonal Balances in terms of Aging in Rabbits (연령증가에 따른 Atrial Natriuretic Peptide의 신장과 호르몬 효과)

  • Kim, Jong-Duk;Kim, Suhn-Hee;Kim, Jung-Soo;Cho, Kyung-Woo
    • The Korean Journal of Physiology
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    • v.23 no.1
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    • pp.51-66
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    • 1989
  • Mammalian cardiocytes secrete atrial natriuretic peptides (ANPs) into plasma, which cause marked natriuresis, diuresis, vasorelaxation and inhibition of hormone secretions. Aging influences the ability of the kidney both to conserve and to excrete sodium; i.e., in old animals, the excretory capacity of sodium is reduced and the time required to excrete sodium load is prolonged. Therefore, it is possible that animals differing in ages may respond differently to ANP. In the present study, we determined whether the renal, hormonal and vascular effects of ANP may be influenced by aging in conscious rabbits. The plasma renin concentration decreased with aging but plasma ANP concentration was significantly lower only in 24-month-old rabbits. Plasma aldosterone concentration and atrial ANP content did not change by aging. In 1-month-old rabbits, ANP (atriopeptin III, 3 ug/kg) administered intravenously caused hypotension and decreased in plasma renin and aldosterone concentrations, but did not cause diuresis and natriuresis. In 2 to 5 month-old rabbits, ANP caused hypotension, decreases in Plasma renin and aldosterone concentrations and marked renal effects. However, in 24-month-old rabbits, all the above effects of ANP was blunted. With hydration of physiological saline at a rate of 15 ml/kg/h for 2hr, urine volume and glomerular filtration rate did not change but the electrolyte excretion as well as fractional excretion of sodium significantly increased. The plasma concentrations of active renin and aldosterone were decreased but plasma inactive renin and ANP concentrations were increased. The changes in renal function and plasma level of hormone showed no differences in different ages. These results suggest that the peripheral vascular receptors to ANP may develop earlier than those in the kidney, and the attenuated vascular and renal responses to ANP in the old age may be due to age-related modifications in renal function and blood vessel.

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Effect of Sodium Intake on Responses of Blood Pressure, Renin-Aldosterone and Renal Excretions to Atrial Natriuretic Peptide in Spontaneously Hypertensive Rats (소금 섭취량을 달리한 정상 및 고혈압쥐에서 Atrial Natriuretic Peptide가 혈압, Renin-Aldosterone 및 신배설에 미치는 영향)

  • Juhn, Jae-Ryang;Lee, Won-Jung;Park, Jae-Sik;Choo, Young-Eun
    • The Korean Journal of Physiology
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    • v.24 no.2
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    • pp.319-329
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    • 1990
  • Effects of atrial natriuretic peptide (ANP) on blood pressure, plasma lenin activity, aldosterone and renal excretion were compared in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar rats fed low, medium or high sodium diet (2, 10, 25 mmol NaCl/100g diet) for 6 weeks. ANP infusion (380 ng/kg/min for 20 min) produced reductions in blood pressure, plasma renin activity, and aldosterone level, but marked increases in hematocrit, urine flow, and excretions of sodium and potassium. The low sodium group showed a significantly enhanced aldosterone lowering effect of ANP than the high sodium group. However, three salt groups showed no difference in effects of ANP on blood pressure, plasma renin activity, hematocrit and diuresis. Natriuretic response to ANP was significantly greater in the high salt-than in the low sait-SHR, but was not different between the Wistar salt groups. There were strain differences in effects of ANP: SHR showed greater responses of blood pressure and natriuresis than Wistar rats. Above results indicate that aldosterone-lowering and natriuretic effects of ANP were modifed by different dietary sodium intakes. However, blood pressure- and renin-lowering, or diuretic effects of ANP were not affected by dietary sodium intakes. The mechanisms whereby dietary sodium intakes alter the effects of ANP in the pathogenesis of hypertension are not clear.

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A Study on Relative Comparison of R&D Performance Using ANP Model (ANP 모델을 이용한 연구개발 성과의 상대적 비교에 대한 연구)

  • Jung, Uk
    • Journal of the Society of Korea Industrial and Systems Engineering
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    • v.33 no.2
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    • pp.89-96
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    • 2010
  • This study explores the application of the analytic network process (ANP) approach for the evaluation of R&D projects with heterogeneous objectives. The ANP model in this study produced the final priorities of projects with respect to several performance measures when there are interdependencies between research objectives and performance measures. The paper provides value to practitioners by providing a generic model for R&D project evaluation. The ANP approach is tested against empirical data drawn from fourteen R&D projects under six different objective programs sponsored by the Korean government.

Application of the Analytic Network Process (ANP) in Importance Analysis of Rural Amenity Resources for Rural Development Project (농촌지역개발사업에 있어서 농촌어메니티자원 중요도 평가를 위한 ANP기법의 활용)

  • Bae, Seung-Jong
    • Journal of The Korean Society of Agricultural Engineers
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    • v.52 no.5
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    • pp.109-118
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    • 2010
  • The objectives of this study are to analyze and compare importance degrees of rural amenity resources for rural development project using AHP and ANP (Analytic Network Process) which can be applied a complex decision making problem. For this study, I chose the 5 rural development project types and the 10 rural amenity resources as major criteria and formed the ANP network from relations with criteria. The importance degree matrix were derived by the results of AHP and several ANP analysis. As the results of this study, the importance degrees of 10 rural amenity resources are determined and the indigenous product resource is identified as the most important resource in general rural development project.

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.

ANP Inhibits Surfactant Secretion from Isoproterenol Stimulated Alveolar Type II Cells

  • Lee, Young-Man
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.1
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    • pp.65-70
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    • 1997
  • In order to investigate the effect of ANP on surfactant secretion from alveolar type II cell(AT II cell) during circulatory derangement in adult respiratory distress syndrome (ARDS), the secretion of surfactant from AT II cells was evaluated in purely isolated AT II cultures from rat lungs. For the simulation of sympathetic stimulation during circulatory derangement, primary AT II cultures were incubatedwith isoproterenol and IBMX. In this isoproterenol stimulated AT II cells, ANP were added in the media for the investigation of effect of ANP on surfactant secretion from AT II cells. For the evaluation of surfactant secretion, $[^3H]-methylcholine$ was incorporated and the level of radiolabelled choline chloride secreted from the cells was determined. As previously reported, isoproterenol and IBMX stimulated surfactant secretion from AT II cells. Isoproterenol showed synergistic increase of surfactant secretion with IBMX in AT II cells. In isoproterenol stimulated AT II cells, physiological level of ANP inhibited the secretion of surfactant in primary cultures of AT II cells. On the basis of these experimental it is suggested that, in association with ciculatory change during ARDS, increased secretion of ANP by the pulmonary edema, hypoxia and congestive heart heart failure might aggravate the symptoms of ARDS by reduction of surfactant secretion from AT II cells.

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[$Ca^{2+}-induced$ $Ca^{2+}$ Release from Sarcoplasmic Reticulum Negatively Regulates Myocytic ANP Release in Beating Rabbit Atria

  • Li, Dan;Quan, He Xiu;Wen, Jin-Fu;Jin, Jing-Yu;Park, Sung-Hun;Kim, Sun-Young;Kim, Sung-Zoo;Cho, Kyung-Woo
    • The Korean Journal of Physiology and Pharmacology
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    • v.9 no.2
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    • pp.87-94
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    • 2005
  • It is not clear whether $Ca^{2+}-induced$ $Ca^{2+}$ release from the sarcoplasmic reticulum (SR) is involved in the regulation of atrial natriuretic peptide (ANP) release. Previously, we have shown that nifedipine increased ANP release, indicating that $Ca^{2+}$ entry via voltage-gated L-type $Ca^{2+}$ channel activation decreases ANP release. The purpose of the present study was two-fold: to define the role of SR $Ca^{2+}$ release in the regulation of ANP release and whether $Ca^{2+}$ entry via L-type $Ca^{2+}$ channel is prerequisite for the SR-related effect on ANP release. Experiments were performed in perfused beating rabbit atria. Ryanodine, an inhibitor of SR $Ca^{2+}$ release, increased atrial myocytic ANP release ($8.69{\pm}3.05$, $19.55{\pm}1.09$, $27.31{\pm}3.51$, and $18.91{\pm}4.76$% for 1, 2, 3, and $6{\mu}M$ ryanodine, respectively; all P<0.01) with concomitant decrease in atrial stroke volume and pulse pressure in a dose-dependent manner. In the presence of thapsigargin, an inhibitor of SR $Ca^{2+}$ pump, ryanodine-induced increase in ANP release was not observed. Thapsigargin attenuated ryanodine-induced decrease in atrial dynamic changes. Blockade of L-type $Ca^{2+}$ channel with nifedipine abolished ryanodine-induced increase in ANP release ($0.69{\pm}5.58$% vs. $27.31{\pm}3.51$%; P<0.001). In the presence of thapsigargin and ryanodine, nifedipine increased ANP release and decreased atrial dynamics. These data suggest that $Ca^{2+}$-induced $Ca^{2+}$ release from the SR is inversely involved in the regulation of atrial myocytic ANP release.