Mechanisms of renal hyporesponsiveness to ANP in heart failure

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چکیده

منابع مشابه

Renal hyporesponsiveness to atrial natriuretic peptide in congestive heart failure results from reduced atrial natriuretic peptide receptor concentrations.

Atrial natriuretic peptide (ANP) and B-type natriuretic peptide decrease blood pressure and cardiac hypertrophy by activating natriuretic peptide receptor A (NPR-A), a transmembrane guanylyl cyclase also known as guanylyl cyclase A. Inactivation of NPR-A is a potential mechanism for the renal hyporesponsiveness observed in congestive heart failure (CHF) but direct data supporting this hypothesi...

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Does the Heart’s Hormone, ANP, Help in Congestive Heart Failure?

In congestive hearf failure, increased secretion of afrial nafriurefic pepfide (ANP) is an important compensatory mechanism that unloads the failing heart and promofes renal salt and wafer excretion. However, acfivafion of opposing sodium-refaining facfors, parficularly the renin-angiofensin sysfem, reduces renal responsiveness to A NP and shifts the cardiovascular sysfem to a state of decompen...

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Pathophysiological Mechanisms and Drugs Leading to Decrease in Renal Function in Congestive Heart Failure

Literature review shows that elevated serum creatinine (or diminished creatinine clearance) is frequent in patients with heart failure (40%) and prognostically bad as it indicates an independently manifold increased mortality. In addition, even renal function worsening during hospitalization (increase in serum creatinine by approximately 30 micromol/L or higher) is not a rare finding (every 4 p...

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Metabolic mechanisms in heart failure.

Although neurohumoral antagonism has successfully reduced heart failure morbidity and mortality, the residual disability and death rate remains unacceptably high. Though abnormalities of myocardial metabolism are associated with heart failure, recent data suggest that heart failure may itself promote metabolic changes such as insulin resistance, in part through neurohumoral activation. A detrim...

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ژورنال

عنوان ژورنال: European Journal of Clinical Investigation

سال: 2003

ISSN: 0014-2972

DOI: 10.1046/j.1365-2362.2003.01222.x