Digitalis increases brain natriuretic peptide in patients with severe congestive heart failure

Ouabain can cause increased secretion of atrial natriuretic peptide (ANP) from atrial cardiocyte culture, but the effects of digitalis in a therapeutic range on the secretion of cardiac natriuretic peptide including ANP and brain natriuretic peptide (BNP), mainly from the ventricle, in patients with...

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Bibliographic Details
Published in:The American heart journal 1997-11, Vol.134 (5), p.910-916
Main Authors: Tsutamoto, Takayoshi, Wada, Atsuyuki, Macda, Keiko, Hisanaga, Tomoko, Fukai, Daisuke, Maeda, Yukiharu, Ohnishi, Masato, Mabuchi, Naoko, Kinoshita, Masahiko
Format: Article
Language:English
Subjects:
Aged
Aldosterone - blood
Angiotensin II - blood
Atrial Natriuretic Factor - blood
Biological and medical sciences
Cardiotonic agents
Cardiotonic Agents - administration & dosage
Cardiotonic Agents - pharmacology
Cardiovascular system
Deslanoside - administration & dosage
Deslanoside - pharmacology
Female
Guanosine Monophosphate - blood
Heart Failure - blood
Heart Failure - drug therapy
Heart Failure - physiopathology
Hemodynamics - drug effects
Humans
Infusions, Intravenous
Male
Medical sciences
Middle Aged
Myocardium - metabolism
Natriuretic Peptide, Brain
Nerve Tissue Proteins - blood
Norepinephrine - blood
Pharmacology. Drug treatments
Renin - blood
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Summary:Ouabain can cause increased secretion of atrial natriuretic peptide (ANP) from atrial cardiocyte culture, but the effects of digitalis in a therapeutic range on the secretion of cardiac natriuretic peptide including ANP and brain natriuretic peptide (BNP), mainly from the ventricle, in patients with congestive heart failure remain to be investigated. Therefore we studied the acute effects of intravenous infusion of a relatively low dose of digitalis or placebo on hemodynamics and neurohumoral factors including the plasma levels of ANP and BNP and cyclic guanosine monophosphate, a second messenger of cardiac natriuretic peptide, in 13 patients with severe congestive heart failure. No significant change in the hemodynamic parameters or neurohumoral factors was observed with placebo. After 1 hour of intravenous administration of deslanoside (0.01 mg/kg), there was a significant decrease of plasma renin activity and angiotensin II, aldosterone, and norepinephrine levels but no significant change of plasma levels of vasopressin and a significant decrease of the pulmonary capillary wedge pressure but no significant change in cardiac index. In addition, plasma levels of ANP (217±47 vs 281±70 pg/ml, p
ISSN:0002-8703
1097-6744
DOI:10.1016/S0002-8703(97)80014-2