Literature DB >> 9115956

Activation of the neuroendocrine response in heart failure: adaptive or maladaptive process?

R Ferrari1, C Ceconi, S Curello, F Ferrari, R Confortini, P Pepi, O Visioli.   

Abstract

Congestive heart failure is a clinical syndrome in which the capacity of the heart to maintain cardiac output is impaired. As a consequence, blood pressure is threatened and endocrine and paracrine mechanisms are activated to preserve circulatory homeostasis and to maintain blood pressure. At terminal stages, a complex multiorgan syndrome develops with severe pump failure, intense systemic vasoconstriction, and avid water and sodium retention. Increasing evidence points to humoral circulating or locally synthesized substances as one of the causes of the terminal consequences of heart failure. Therefore, the hypothesis that the syndrome of heart failure is, at least in part, a humoral disease has developed and is obtaining scientific credibility. Consequently, the neuroendocrine response to heart failure is no longer viewed as a compensatory beneficial mechanism. Instead, we have learned through the years that pharmacological treatment aimed at reducing the effect of the neuroendocrine response is indeed clinically and prognostically advantageous for the patient.

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Year:  1996        PMID: 9115956     DOI: 10.1007/bf00052509

Source DB:  PubMed          Journal:  Cardiovasc Drugs Ther        ISSN: 0920-3206            Impact factor:   3.727


  57 in total

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Authors:  B Levine; J Kalman; L Mayer; H M Fillit; M Packer
Journal:  N Engl J Med       Date:  1990-07-26       Impact factor: 91.245

Review 2.  Atrial natriuretic hormone, the renin-aldosterone axis, and blood pressure-electrolyte homeostasis.

Authors:  J H Laragh
Journal:  N Engl J Med       Date:  1985-11-21       Impact factor: 91.245

Review 3.  Congestive cardiac failure: central role of the arterial blood pressure.

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Journal:  Br Heart J       Date:  1987-09

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Authors:  R Ferrari; C Ceconi; F De Giuli; A Panzali; P Harris
Journal:  Cardioscience       Date:  1992-03

5.  The effects of ACE inhibitors on exercise capacity in the treatment of congestive heart failure.

Authors:  G A Riegger
Journal:  J Cardiovasc Pharmacol       Date:  1990       Impact factor: 3.105

6.  The neurohormonal hypothesis: a theory to explain the mechanism of disease progression in heart failure.

Authors:  M Packer
Journal:  J Am Coll Cardiol       Date:  1992-07       Impact factor: 24.094

7.  Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts.

Authors:  M R Bristow; R Ginsburg; W Minobe; R S Cubicciotti; W S Sageman; K Lurie; M E Billingham; D C Harrison; E B Stinson
Journal:  N Engl J Med       Date:  1982-07-22       Impact factor: 91.245

8.  Cellular mechanisms for synthesis and secretion of atrial natriuretic peptide and brain natriuretic peptide in cultured rat atrial cells.

Authors:  E Suzuki; Y Hirata; O Kohmoto; T Sugimoto; H Hayakawa; H Matsuoka; T Sugimoto; M Kojima; K Kangawa; N Minamino
Journal:  Circ Res       Date:  1992-11       Impact factor: 17.367

9.  Plasma norepinephrine as an indicator of sympathetic neural activity in clinical cardiology.

Authors:  D S Goldstein
Journal:  Am J Cardiol       Date:  1981-12       Impact factor: 2.778

10.  Effects of isoproterenol (I) on the release of atrial natriuretic peptide (ANP) from isolated atria.

Authors:  G Agnoletti; C Ceconi; L Comini; R Ferrari; S Curello; C Scotti; A F Panzali
Journal:  Am J Cardiovasc Pathol       Date:  1992
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  2 in total

Review 1.  Blood coagulation in patients with chronic heart failure: evidence for hypercoagulable state and potential for pharmacological intervention.

Authors:  Ferruccio De Lorenzo; Neelam Saba; Vijay V Kakkar
Journal:  Drugs       Date:  2003       Impact factor: 9.546

Review 2.  Molecular and cellular mechanisms of cardiotoxicity.

Authors:  Y J Kang
Journal:  Environ Health Perspect       Date:  2001-03       Impact factor: 9.031

  2 in total

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