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Cardiac failure atrial natriuretic peptide

In the example of a-human atrial natriuretic peptide (ANP), found at increased plasma levels in patients with heart failure, Numata et al. [70] demonstrated how IPCR sensitivity accelerated conventional assay procedures. For individual treatment of the cardiac patients, a prompt detection of atrial distension by the presence of the ANP marker would be desirable. Common ANP tests, however, take 2-3 days for the quantification of plasma by radiometric or ELISA techniques. With sandwich IPCR, the assay time could be shortened to 5 hours. A good correlation between IPCR and radiometric detection was maintained, combined with an additional improvement of the detection limit to 2 ng/L ANP. The average level of ANP in plasma for 25 patients with heart failure was found to be 117 100 ng/L, significantly higher than the typical level of 20 14 ng/L for healthy subjects. [Pg.281]

NESIRITIDE Nesiritide (natrecor), a recombinant form of human brain natriuretic peptide (BNP), is FDA-approved for treatment of dyspnea due to congestive heart failure. The natriuretic peptides—atrial natriuretic peptide (ANP), BNP, and C-type natriuretic peptide—are a family of endogenous hormones that possess potent natriuretic, diuretic, and vasodilator properties. BNP is secreted by ventricular cardiac myocytes in response to stretch circulating levels of BNP correlate with the severity of heart failure. In the setting of heart failure, the effects of BNP counteract the effects of Angll and NE by producing vasodilation, natriuresis, and diuresis. [Pg.571]

C) Atrial natriuretic peptide increases cardiac contractility in congestive heart failure... [Pg.171]

Numerous neuroendocrine biomarkers correlate with severity of cardiac dysfunction. Heart failure is associated with increase in peripheral vascular resistance due to increases in sympathetic tone, norepinephrine, renin, angiotensin II, arginine vasopressin, and endothelin-1. The increased venous pressure causes atrial distension that stimulates production and release of atrial and brain natriuretic peptides (ANP, BNP) from the atria and ventricles, respectively. ANP inhibits the renin-angiotensin-aldosterone system. In humans and mammals, BNP has been found to be an early biomarker of left ventricular hypertrophy developing with doxorubicin cardiotoxicity, congestive heart failure, or occult dilated cardiomyopathy (Erkus et al. 2006 Walker 2006 Oyama, Sisson, and Solter 2007). [Pg.151]


See other pages where Cardiac failure atrial natriuretic peptide is mentioned: [Pg.37]    [Pg.37]    [Pg.1630]    [Pg.419]    [Pg.487]    [Pg.119]   
See also in sourсe #XX -- [ Pg.169 ]




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