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  • 1
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    Online Resource
    Ventricular adrenomedullin concentration is a sensitive biochemical marker for volume and pressure overload in rats
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 278, No. 2 ( 2000-02-01), p. H633-H642
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 278, No. 2 ( 2000-02-01), p. H633-H642
    Abstract: This study was designed to investigate the pathophysiological significance of adrenomedullin (AM) concentration in volume- and pressure-overloaded cardiac hypertrophy. We measured ventricular AM concentrations and compared them with changes of α-actin and myosin heavy chain (MHC) mRNA isoforms after the creation of an aortocaval (AC) shunt as a volume-overload model or the injection of monocrotaline (MCT) as a pressure-overload model, respectively. The left ventricular AM levels after the creation of AC shunt and the right ventricular AM levels after the injection of MCT were significantly increased and correlated with changes of the α-actin and MHC mRNA isoforms. However, the ventricular AM mRNA expressions were increased and correlated with ventricular AM concentrations only in the AC shunt model. These results suggest that the ventricular AM levels are upregulated in both the volume- and pressure-overloaded cardiac hypertrophy by differential transcriptional regulation and that the ventricular AM may be a biochemical marker for the volume and pressure overload to the ventricle.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.2000.278.2.H633
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 2
    Online Resource
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    Increased cardiac levels of nitric oxide in patients with chronic heart failure
    Elsevier BV ; 2000
    In:  The American Journal of Cardiology Vol. 86, No. 4 ( 2000-08), p. 474-477
    Details
    In: The American Journal of Cardiology, Elsevier BV, Vol. 86, No. 4 ( 2000-08), p. 474-477
    Type of Medium: Online Resource
    ISSN: 0002-9149
    URL: Article
    DOI: 10.1016/S0002-9149(00)00973-5
    RVK:
    XA 18500
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2000
    detail.hit.zdb_id: 2019595-3
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  • 3
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    Online Resource
    Effect of neutral endopeptidase inhibitor on endogenous atrial natriuretic peptide as a paracrine factor in cultured cardiac fibroblasts
    Wiley ; 2000
    In:  British Journal of Pharmacology Vol. 131, No. 6 ( 2000-11), p. 1204-1210
    Details
    In: British Journal of Pharmacology, Wiley, Vol. 131, No. 6 ( 2000-11), p. 1204-1210
    Abstract: Cardiac remodelling is a fundamental response to hypertension, myocardial infarction and chronic heart failure, and involves cardiac fibroblast proliferation and production of extracellular matrix components such as collagen. The present study was performed to examine the role of endogenous atrial natriuretic peptide (ANP) as a possible paracrine factor for cardiac fibroblasts, and to examine the effects of three neutral endopeptidase (NEP) inhibitors, thiorphan, phosphoramidon and ONO‐BB‐039‐02 (ONO‐BB) on endogenous ANP‐induced changes in collagen synthesis by cultured neonatal rat cardiac fibroblasts. Each NEP inhibitor singly had no significant effect on collagen synthesis by cardiac fibroblasts, except for maximum concentration (10 −3   M ) of thiorphan. Exogenous ANP inhibited collagen synthesis in a concentration‐dependent manner (10 −8 –10 −6   M ). Thiorphan (10 −4 and 10 −3   M ) and phosphoramidon (10 −5 and 10 −4   M ) enhanced the ANP (10 −7   M )‐induced decrease in collagen synthesis. ONO‐BB (10 −5 and 10 −4   M ) slightly enhanced the ANP‐induced decrease in collagen synthesis. Myocyte‐conditioned medium (MC‐CM), as well as exogenous ANP, inhibited collagen synthesis dose‐dependently. The decrease in collagen synthesis at 100% MC‐CM was augmented by thiorphan (10 −3   M ), phosphoramidon (10 −4   M ) and ONO‐BB (10 −4   M ). HS‐142‐1, a natriuretic peptide receptor antagonist, significantly reduced the MC‐CM plus thiorphan‐ and MC‐CM plus ONO‐BB‐induced decrease in collagen synthesis, by 92 and 62%, respectively and showed a tendency to attenuate the MC‐CM plus phosphoramidon‐induced decrease in collagen synthesis by 40%. Our observations suggested that endogenous ANP released from cardiomyocytes inhibited collagen synthesis as a paracrine factor and that NEP inhibitors enhanced the activity of this peptide in cardiac fibroblasts. British Journal of Pharmacology (2000) 131 , 1204–1210; doi: 10.1038/sj.bjp.0703679
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Article
    DOI: 10.1038/sj.bjp.0703679
    Language: English
    Publisher: Wiley
    Publication Date: 2000
    detail.hit.zdb_id: 2029728-2
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    Inhibitory Regulation of Hypertrophy by Endogenous Atrial Natriuretic Peptide in Cultured Cardiac Myocytes
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 35, No. 1 ( 2000-01), p. 19-24
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. 1 ( 2000-01), p. 19-24
    Abstract: Abstract —Atrial natriuretic peptide (ANP) may function as an endogenous regulator of cardiac hypertrophy, because the natriuretic peptide receptor has been found in the heart and because mice lacking its receptor have been shown to have a markedly elevated ventricular mass. We examined the role of endogenous ANP in cardiac hypertrophy in vitro. The effects of the blockade of endogenous ANP by its receptor antagonist, HS-142–1, on cell hypertrophy were investigated with the use of cultured neonatal rat ventricular myocytes. HS-142–1 increased the basal and phenylephrine (PE, 10 −5 mol/L)–stimulated protein syntheses in a concentration-dependent manner (1 to 300 μg/mL). A significant increase in the cell size of myocytes was also induced by this antagonist. In addition, the expression levels of skeletal α-actin, β-myosin heavy chain, and ANP genes, markers of hypertrophy, were partially elevated by treatment with HS-142–1 (100 μg/mL) under nonstimulated or PE-stimulated conditions. A cGMP-specific phosphodiesterase inhibitor, zaprinast (5×10 −4 mol/L), and a cGMP analogue (10 −4 mol/L) suppressed the basal and PE-stimulated protein syntheses. Our observations suggest that endogenous ANP inhibits cardiac myocyte hypertrophy under basal and PE-stimulated conditions, probably through a cGMP-dependent process. ANP may play a role as an autocrine factor in the regulation of cardiac myocyte growth.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.35.1.19
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 2094210-2
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  • 5
    Online Resource
    Online Resource
    Cardiac adrenomedullin gene expression and peptide accumulation after acute myocardial infarction in rats
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 278, No. 4 ( 2000-04-01), p. R1019-R1026
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 278, No. 4 ( 2000-04-01), p. R1019-R1026
    Abstract: Plasma adrenomedullin (AM) has been shown to increase in the early phase of acute myocardial infarction (MI). However, little information is available regarding cardiac AM synthesis after MI. Accordingly, we examined the time course of ventricular AM production and potential stimulation of AM in the infarcted and noninfarcted regions in MI rats produced by coronary artery ligation. Compared with sham-operated rats, the ventricular AM peptide level 6 h after MI increased 1.5-fold in the infarcted region and 1.7-fold in the noninfarcted region in association with increased left ventricular end-diastolic pressure (EDP). Northern blot analysis also showed marked induction of AM gene expression in the infarcted region (11-fold) and the noninfarcted region (6-fold) 6 h after MI. The AM peptide level in the infarcted region reached its peak (2.6-fold) 1 wk postinfarction and thereafter decreased to normal. In the noninfarcted region, however, the AM level remained elevated for at least 4 wk. Immunohistochemical studies demonstrated that intense immunostaining for AM was limited to myocytes in both the infarcted and noninfarcted regions. Interestingly, the AM level in the noninfarcted region correlated positively with infarct size ( r = 0.40, P  〈  0.01) and EDP ( r = 0.52, P  〈  0.001). An oral angiotensin-converting enzyme inhibitor suppressed the overproduction of AM 1 wk postinfarction in association with decreases in EDP and mean arterial pressure. In summary, cardiac AM synthesis was rapidly induced in both the infarcted and noninfarcted regions after MI. The subsequent ventricular AM in the two regions demonstrated different time-concentration curves during 4 wk after MI. AM may be synthesized predominantly by cardiac myocytes, but not by fibroblasts, at least in part, in association with increased ventricular load after MI.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.2000.278.4.R1019
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Urocortin, a member of the corticotropin-releasing factor family, in normal and diseased heart
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 279, No. 6 ( 2000-12-01), p. H3031-H3039
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 279, No. 6 ( 2000-12-01), p. H3031-H3039
    Abstract: In the present study we investigated the form of expression, action, second messenger, and the cellular location of urocortin, a member of the corticotropin-releasing factor (CRF) family, in the heart. Urocortin mRNA, as shown by quantitative RT-PCR analysis, is expressed in the cultured rat cardiac nonmyocytes (NMC) as well as myocytes (MC) in the heart, whereas CRF receptor type 2β (CRF-R2β), presumed urocortin receptor mRNA, is predominantly expressed in MC compared with NMC. Urocortin mRNA expression is higher in left ventricular (LV) hypertrophy than in normal LV, whereas CRF-R2β mRNA expression is markedly depressed in LV hypertrophy compared with normal LV. Urocortin more potently increased the cAMP levels in both MC and NMC than did CRF, and its effect was more potent in MC than in NMC. Urocortin significantly increased protein synthesis by [ 14 C]Phe incorporations and atrial natriuretic peptide secretion in MC and collagen and increased DNA synthesis by [ 3 H]prolin and [ 3 H]Thy incorporations in NMC. An immunohistochemical study revealed that urocortin immunoreactivity was observed in MC in the normal human heart and that it was more intense in the MC of the human failing heart than in MC of the normal heart. These results, together with the recent evidence of urocortin for positive inotropic action, suggest that increased urocortin in the diseased heart may modulate the pathophysiology of cardiac hypertrophy or failing heart, at least in part, via cAMP signaling pathway.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.2000.279.6.H3031
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Preservation of the right atrial appendage improves reduced plasma atrial natriuretic peptide levels after the maze procedure
    Elsevier BV ; 2000
    In:  The Journal of Thoracic and Cardiovascular Surgery Vol. 119, No. 4 ( 2000-04), p. 790-794
    Details
    In: The Journal of Thoracic and Cardiovascular Surgery, Elsevier BV, Vol. 119, No. 4 ( 2000-04), p. 790-794
    Type of Medium: Online Resource
    ISSN: 0022-5223
    URL: Article
    DOI: 10.1016/S0022-5223(00)70015-8
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2000
    detail.hit.zdb_id: 2007600-9
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