scholarly journals I027 Circulating levels of cardiac natriuretic peptides measured by highly sensitive and specific IRMA methods in normal subjects and in patients with heart failure

1998 ◽  
Vol 11 (4) ◽  
pp. 174A
Author(s):  
A CLERICO
Keyword(s):  
Heart Failure ◽  
Natriuretic Peptides ◽  
Normal Subjects ◽  
Highly Sensitive ◽  
Patients With Heart Failure ◽  
Cardiac Natriuretic Peptides ◽  
Circulating Levels

Cardiac natriuretic hormones, neuro-hormones, thyroid hormones and cytokines in normal subjects and patients with heart failure

2004 ◽  
Vol 42 (6) ◽  
Author(s):  
Michele Emdin ◽  
Claudio Passino ◽  
Concetta Prontera ◽  
Annalisa Iervasi ◽  
Andrea Ripoli ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Thyroid Hormones ◽  
Natriuretic Peptide ◽  
Nyha Class ◽  
Normal Subjects ◽  
Clinical Severity ◽  
Tnf Α ◽  
Patients With Heart Failure ◽  
Circulating Levels

AbstractThe derangement of neuro-endocrine control of circulation influences both disease evolution and response to treatment in patients with heart failure, but little data are available about the complex relationships between the degree of neuro-hormonal activation and clinical severity. We studied the relationships between cardiac natriuretic hormones (CNHs) and several neuro-hormones and immunological markers in a prospective cohort of 105 consecutive patients with cardiomyopathy (77 men and 28 women, mean age 66.7±12.4 years, range 33–89 years). We assayed the circulating levels of CNHs (atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)), plasma renin activity (PRA), aldosterone, cortisol, adrenaline, noradrenaline, thyroid hormones and thyroid stimulating hormone (TSH), tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6). The concentrations of all CNHs and neuro-hormones were higher in patients with heart failure compared to normal subjects, except for free triiodothyronine (FT3), which was below normal values. ANP was positively related to NYHA class, IL-6, adrenaline, noradrenaline and cortisol, while negatively with ejection fraction and FT3. BNP was positively related to age, NYHA class, IL-6, TNF-α, adrenaline, noradrenaline and cortisol, while negatively with ejection fraction and FT3. A stepwise multiple linear regression indicated that plasma ANP depended only on ejection fraction, adrenaline and noradrenaline values, while for plasma BNP variation NYHA class contributed too. Our data confirm a progressive activation of hormonal and immunological systems in patients with heart failure. Furthermore, CNH circulating levels in heart failure are affected not only by cardiac function and disease severity, but also by activation of neuro-hormonal and stress-related cytokine systems, as well as by the thyroid hormones, even on usual medical treatment.

Cardiac Natriuretic Peptides in Heart Failure

1993 ◽  
Vol 25 (6) ◽  
pp. 503-505 ◽  
Author(s):  
M. Gary Nicholls ◽  
A. Mark Richards ◽  
Ian G. Crozier ◽  
Eric A. Espiner ◽  
Hamid Ikram
Keyword(s):  
Heart Failure ◽  
Natriuretic Peptides ◽  
Cardiac Natriuretic Peptides

scholarly journals Circulating levels of linoleic acid and HDL-cholesterol are major determinants of 4-hydroxynonenal protein adducts in patients with heart failure

Redox Biology ◽  
2014 ◽  
Vol 2 ◽  
pp. 148-155 ◽  
Author(s):  
Caroline Asselin ◽  
Anique Ducharme ◽  
Thierry Ntimbane ◽  
Matthieu Ruiz ◽  
Annik Fortier ◽  
...  
Keyword(s):  
Heart Failure ◽  
Linoleic Acid ◽  
Hdl Cholesterol ◽  
Protein Adducts ◽  
Patients With Heart Failure ◽  
Circulating Levels

The renal and cardiovascular effects of natriuretic peptides

2017 ◽  
Vol 41 (2) ◽  
pp. 179-185 ◽  
Author(s):  
Philip Ching Yat Wong ◽  
Jun Guo ◽  
Aidong Zhang
Keyword(s):  
Heart Failure ◽  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Plasma Levels ◽  
Cardiovascular Effects ◽  
Target Cells ◽  
Natriuretic Peptide Receptor ◽  
Peptide Receptor ◽  
Endocrine Organs ◽  
Patients With Heart Failure

The landmark report by de Bold et al. in 1981 signified the heart as one of the endocrine organs involved in fluid and salt balance (de Bold AJ, Borenstein HB, Veress AT, Sonnenberg H. Life Sci 28: 89–94, 1981). Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are secreted from cardiomyocytes in response to cardiac stretch as in the case of heart failure, whereas C-type natriuretic peptide (CNP) is secreted from endothelial and renal cells in response to cytokines and endothelium-dependent agonists, such as acetylcholine. Binding ANP or BNP to natriuretic peptide receptor A induces cyclic guanylyl monophosphate as second messenger in the target cells to mediate the following: natriuresis; water diuresis; increasing glomerular filtration rate; decreasing systemic sympathetic activities; plasma volume; cardiac output and blood pressure; and curbing mitoses of heart fibroblasts and hypertrophy of cardiovascular muscle cells. ANP, BNP, and CNP are cleared from the bloodstream by natriuretic peptide receptor C and degraded by an ectoenzyme called neprilysin (NEP). The plasma levels of BNP are typically >100 pg/ml in patients with congestive heart failure. Sacubitril/valsartan is an angiotensin receptor NEP inhibitor that prevents the clinical progression of surviving patients with heart failure more effectively than enalapril, an angiotensin-converting enzyme inhibitor. A thorough understanding of the renal and cardiovascular effects of natriuretic peptides is of major importance for first-year medical students to gain insight into the significance of plasma levels of BNP in patients with heart failure.

Peripheral muscle ergoreceptors and ventilatory response during exercise recovery in heart failure

1999 ◽  
Vol 276 (3) ◽  
pp. H913-H917 ◽  
Author(s):  
Noelle Francis ◽  
Alain Cohen-Solal ◽  
Damien Logeart
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Exercise Recovery ◽  
Cuff Inflation ◽  
Half Time ◽  
Peripheral Muscle ◽  
Patients With Heart Failure ◽  
Kinetics Of

Recent studies have suggested that the increased ventilatory response during exercise in patients with chronic heart failure was related to the activation of muscle metaboreceptors. To address this issue, 23 patients with heart failure and 7 normal subjects performed arm and leg bicycle exercises with and without cuff inflation around the arms or the thighs during recovery. Obstruction slightly reduced ventilation and gas exchange variables at recovery but did not change the kinetics of recovery of these parameters compared with nonobstructed recovery: half-time of ventilation recovery was 175 ± 54 to 176 ± 40 s in patients and 155 ± 66 to 127 ± 13 s in controls ( P < 0.05, patients vs. controls, not significant within each group from baseline to obstructed recovery). We conclude that muscle metaboreceptor activation does not seem to play a role in the exertion hyperventilation of patients with heart failure.

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