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      KCI등재 SCIE SCOPUS

      Changes of Atrial Natriuretic Peptide System in Rats with Puromycin Aminonucleoside-Induced Nephrotic Syndrome

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      https://www.riss.kr/link?id=A103917866

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      다국어 초록 (Multilingual Abstract)

      Sodium retention is a hallmark of nephrotic syndrome. We investigated whether sodium retention is associated with changes of natriuretic peptide system at different stages (i.e., a sodium retaining stage and a compensatory stage) of nephrotic syndrome...

      Sodium retention is a hallmark of nephrotic syndrome. We investigated whether sodium retention is associated with changes of natriuretic peptide system at different stages (i.e., a sodium retaining stage and a compensatory stage) of nephrotic syndrome. At day 7 after PAN (puromycin aminonucleoside) injection, the urinary excretion of sodium was decreased, along with the development of ascites and positive sodium balance. The plasma and urinary ANP (atrial natriuretic peptide) immunoreactivities were increased. ANP mRNA expression was increased in the heart and kidney, whereas that of NPR (natriuretic peptide receptor)-A and NPR-C mRNA was decreased in the kidney. The expression of NEP was decreased in the kidney. At day 14, urinary excretion of sodium did not differ from the control. The plasma ANP level and heart ANP mRNA expression returned to their control values. The expression of ANP mRNA in the kidney was increased in association with increased urinary ANP immunoreactivities. The expression of NPR-A in the kidney became normal, whereas that of NPR-C kept decreased. The expression of NEP (neutral endopeptidase) remained decreased. These findings suggest that the increased renal ANP synthesis in association with decreased metabolism via NEP and NPR-C may play a compensatory role against the development of sodium retention in nephrotic syndrome. The decreased of NPR-A expression in the kidney may contribute to the ANP resistance at day 7. The subsequent recovery of NPR-A expression may play a role in promoting sodium excretion in later stage (at day 14).

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      참고문헌 (Reference)

      1 Wilkins MR, "The natriuretic-peptide family" 349 : 1307-1310, 1997

      2 Drewett JG, "The family of guanylyl cyclase receptors and their ligands" 15 : 135-162, 1994

      3 Ichikawa I, "Role for intrarenal mechanisms in the impaired salt excretion of experimental nephritic syndrome" 71 : 91-103, 1983

      4 Goetz KL, "Reinhardt HW. Atrial stretch increases sodium excretion independently of release of atrial peptides" 250 : R946-R950, 1986

      5 Vande Walle JG, "Pathogenesis of edema formation in the nephrotic syndrome" 16 : 283-293, 2001

      6 Parkes DG, "Long-term hemodynamic actions of atrial natriuretic factor (99-126) in conscious sheep" 254 : H811-H815, 1988

      7 Deschenes G, "Increased synthesis and avp unresponsiveness of Na,K-ATPase in collecting duct from nephrotic rats" 12 : 2241-2252, 2001

      8 Kim SW, "Increased expression and apical targeting of renal ENaC subunits in puromycin aminonucleoside-induced nephrotic syndrome in rats" 286 : F922-F935, 2004

      9 Kim SW, "Increased apical targeting of renal epithelial sodium channel subunits and decreased expression of type 2 11beta-hydroxysteroid dehydrogenase in rats with CCl4-induced decompensated liver cirrhosis" 16 : 3196-3210, 2005

      10 Woolf AS, "Effects of physiological infusion of atrial natriuretic factor on healthy subjects and patients with the nephrotic syndrome" 52 : 244-250, 1989

      1 Wilkins MR, "The natriuretic-peptide family" 349 : 1307-1310, 1997

      2 Drewett JG, "The family of guanylyl cyclase receptors and their ligands" 15 : 135-162, 1994

      3 Ichikawa I, "Role for intrarenal mechanisms in the impaired salt excretion of experimental nephritic syndrome" 71 : 91-103, 1983

      4 Goetz KL, "Reinhardt HW. Atrial stretch increases sodium excretion independently of release of atrial peptides" 250 : R946-R950, 1986

      5 Vande Walle JG, "Pathogenesis of edema formation in the nephrotic syndrome" 16 : 283-293, 2001

      6 Parkes DG, "Long-term hemodynamic actions of atrial natriuretic factor (99-126) in conscious sheep" 254 : H811-H815, 1988

      7 Deschenes G, "Increased synthesis and avp unresponsiveness of Na,K-ATPase in collecting duct from nephrotic rats" 12 : 2241-2252, 2001

      8 Kim SW, "Increased expression and apical targeting of renal ENaC subunits in puromycin aminonucleoside-induced nephrotic syndrome in rats" 286 : F922-F935, 2004

      9 Kim SW, "Increased apical targeting of renal epithelial sodium channel subunits and decreased expression of type 2 11beta-hydroxysteroid dehydrogenase in rats with CCl4-induced decompensated liver cirrhosis" 16 : 3196-3210, 2005

      10 Woolf AS, "Effects of physiological infusion of atrial natriuretic factor on healthy subjects and patients with the nephrotic syndrome" 52 : 244-250, 1989

      11 Perico N, "Edema of the nephrotic syndrome: the role of the atrial natriuretic peptide system" 22 : 355-366, 1993

      12 Singer DR, "Dissociation between plasma atrial natriuretic peptide levels and urinary sodium excretion after intravenous saline infusion in normal man" 73 : 285-289, 1987

      13 Deschenes G, "Collecting duct Na,K-ATPase activity correlates with urinary sodium excretion in rat nephrotic syndrome" 11 : 604-615, 2000

      14 Valentin JP, "Cellular basis for blunted volume expansion natriuresis in experimental nephrotic syndrome" 90 : 1302-1312, 1992

      15 Perico N, "Blunted excretory response to atrial natriuretic peptide in experimental nephrosis" 36 : 57-64, 1989

      16 Kim SW, "Biphasic changes of epithelial sodium channel abundance and trafficking in common bile duct ligation-induced liver cirrhosis" 69 : 89-98, 2006

      17 Peterson C, "Atrial natriuretic peptide and the renal response to hypervolemia in nephrotic humans" 34 : 825-831, 1988

      18 Livak KJ, "Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method" 25 : 402-408, 2001

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-04-29 학술지명변경 외국어명 : THE KOREAN JOURNAL OF Physiology & Pharmacology -> The Korean Journal of Physiology & Pharmacology KCI등재
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2011-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2009-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2007-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2006-10-12 학술지명변경 한글명 : 대한 생리.약리학회지 -> The Korean Journal of Physiology & Pharmacology
      외국어명 : THE KOREAN JOURNAL OF Physilogy & Pharmacology -> THE KOREAN JOURNAL OF Physiology & Pharmacology
      KCI등재
      2004-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2003-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2001-07-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 1.85 0.36 1.29
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      1.05 0.9 0.575 0.09
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