Endothelin-1, endothelin-1 receptors and cardiac natriuretic peptides in failing human heart.

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  • Additional Information
    • Source:
      Publisher: Elsevier Country of Publication: Netherlands NLM ID: 0375521 Publication Model: Print Cited Medium: Print ISSN: 0024-3205 (Print) Linking ISSN: 00243205 NLM ISO Abbreviation: Life Sci Subsets: MEDLINE
    • Publication Information:
      Publication: <2008->: Amsterdam : Elsevier
      Original Publication: Oxford; Elmsford, N. Y. [etc.] Pergamon Press.
    • Subject Terms:
      Atrial Natriuretic Factor/*biosynthesis ; Endothelin-1/*analysis ; Heart Failure/*metabolism ; Myocardium/*metabolism ; Natriuretic Peptide, Brain/*biosynthesis ; Receptors, Endothelin/*analysis; Adult ; Female ; Humans ; Male ; Receptor, Endothelin A ; Receptor, Endothelin B
    • Abstract:
      Endothelin (ET)-1 is a potent vasoconstrictor peptide produced in the myocardium that can exert important effects on cardiac myocyte growth and phenotype; cardiac natriuretic peptides (ANP and BNP) are known to act as physiological antagonists of ET-1. In this study a comparative determination of ET-1 receptors and of the local productions of ET-1 and of ANP and BNP was made in different sites of failing and nonfailing hearts. Tissue from right and left atrium, right and left ventricle and interventricular septum from seven adult heart transplant recipients with end-stage idiopathic dilated cardiomyopathy (functional class III and IV, with ejection fraction < 35%) and from four postmortem subjects without cardiac complications was analyzed. In failing hearts we observed a tendency to increase of density of binding sites, most evident in left ventricle (62.6+/-22.6 fmol/mg protein vs. 29.0+/-3.3, mean +/- SEM, p = ns). A prevalence of ET-A subclass, observed in all samples, resulted more pronounced in failing hearts where this increase, found in all the cardiac regions, was more evident in left ventricle (p = 0.0007 vs nonfailing hearts). The local concentrations of ET-1, ANP and BNP resulted significantly increased in failing hearts with respect to controls in all sides of the heart. In failing hearts we have observed a tendency to increase in endothelin receptor density mainly due to a significant upregulation of ET-A subtype and a parallel increase of the tissue levels of ANP, BNP and ET-1 indicating an activation of these systems in heart failure.
    • Accession Number:
      0 (Endothelin-1)
      0 (Receptor, Endothelin A)
      0 (Receptor, Endothelin B)
      0 (Receptors, Endothelin)
      114471-18-0 (Natriuretic Peptide, Brain)
      85637-73-6 (Atrial Natriuretic Factor)
    • Publication Date:
      Date Created: 20010613 Date Completed: 20010628 Latest Revision: 20190701
    • Publication Date:
      20231215
    • Accession Number:
      10.1016/s0024-3205(01)01076-1
    • Accession Number:
      11400914