Effects of propranolol and pindolol on plasma ANP levels in humans at rest and during exercise

Bouissou, P.; Galen, F. X.; Richalet, Jean‐Paul; Lartigue, M; Devaux, Floriane; Dubray, Claude; Atlan, G

doi:10.1152/ajpregu.1989.257.2.r259

Cited by 14 publications

(11 citation statements)

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“…The effect of BB on plasma NP has been reported in population-based studies, 15 in healthy control subjects, 16 during exercise, in hypertension, 17,18 in coronary disease, 19 and in HF. 20 -30 The reported responses are widely divergent, presumably reflecting differences between specific ␤-blockers and the effects of dose and duration of treatment and clinical state.…”

Section: Clinical Perspective P 985mentioning

confidence: 95%

Introduction of Metoprolol Increases Plasma B-Type Cardiac Natriuretic Peptides in Mild, Stable Heart Failure

et al. 2006

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Background-The effect of ␤-blockade on the cardiac natriuretic peptides is poorly understood but could contribute to their beneficial treatment effect and may be relevant to clinical use of plasma brain natriuretic peptide (BNP)/N-terminal pro brain natriuretic peptide (NTproBNP) measurements in risk stratification and in titration of anti-heart failure therapy. Methods and Results-Sixteen men with mild, stable heart failure (NYHA class II to III; left ventricular ejection fraction Ͻ40%) underwent serial blood sampling for plasma natriuretic peptide levels and received infusions of atrial natriuretic peptide (ANP) and BNP before and 6 weeks after the introduction and uptitration of metoprolol or 6 weeks unchanged therapy in a randomized, parallel-group design. Plasma natriuretic peptides (BNP, NTproBNP, ANP, and NTproANP) were increased by metoprolol (PϽ0.01 for all). The natriuretic responses to ANP and BNP infusions were sustained with the introduction of metoprolol despite reduced renal perfusion pressure. The levels of the noninfused natriuretic peptide were increased by both ANP and BNP infusions, and this effect was enhanced by metoprolol. The early plasma half-life (t 1 ⁄2␣) of BNP was prolonged by metoprolol (5.6Ϯ0.45 to 11Ϯ1.3 versus 5.7Ϯ0.8 to 6.6Ϯ1.3 minutes in control subjects; Pϭ0.019). Conclusions-Plasma cardiac natriuretic peptide levels increase significantly with the introduction of metoprolol in heart failure as a result of effects on secretion and clearance. Natriuretic responses to NP infusions are sustained with ␤-blockade despite reduced renal perfusion pressure. Clinicians should be aware that the introduction of metoprolol causes a rise in plasma BNP/NTproBNP that is unrelated to deterioration in clinical status and must be considered when measurements are undertaken for risk stratification or titration of treatment.

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Section: Clinical Perspective P 985mentioning

confidence: 95%

Introduction of Metoprolol Increases Plasma B-Type Cardiac Natriuretic Peptides in Mild, Stable Heart Failure

et al. 2006

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“…Indeed, ACE inhibitors, valsartan, diuretics, and nitrates have been shown to reduce plasma CNH concentrations in parallel with hemodynamic and clinical improvement (34, 84, 130, 136 -144 ). More variable effects on plasma CNH concentrations have been reported after ␤-blockade and are at least in part attributable to their differing specificities or to ancillary properties (34,84,90,132,137,(145)(146)(147)(148). Acute administration of ␤-blockers may provide an early increase in plasma CNHs, whereas sustained treatment with associated improvement in cardiac function and reduction in filling pressure and cardiac volumes should be associated with a decrease in hormone concentrations (34 ).…”

Section: Cnh Assays In the Follow-up Of Patients With Hfmentioning

confidence: 99%

Diagnostic Accuracy and Prognostic Relevance of the Measurement of Cardiac Natriuretic Peptides: A Review

2004

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Background:The pathophysiologic and clinical relevance of cardiac natriuretic hormone (CNH) assays has been investigated in numerous experimental and clinical studies. Authors have sought to evaluate the diagnostic accuracy and prognostic relevance of the measurement of CNHs according to evidence-based laboratory medicine principles. Methods: In June 2003, we ran a computerized literature search on National Library of Medicine using keywords "ANP" and "BNP" and found more than 12 300 and 1200 articles, respectively. A more refined search with keywords "ANP or BNP assay" extracted ϳ7000 and 800 articles, respectively. Only studies specifically designed to evaluate the diagnostic accuracy and prognostic relevance of CNH measurements were selected from this huge mass of articles to be discussed in this review. Content: Several studies suggested that CNH assays may be clinically useful for the screening and classification of patients with heart failure, as a prognostic marker in cardiovascular disease, in the follow-up of patients with heart failure, and because they may reduce the need for further cardiac investigation. However, it is difficult to compare even the best-designed studies because not only did the authors evaluate different populations, they also used different gold standards. Conclusions: CNH assays and conventional diagnostic work-ups provide complementary information for evaluation of the presence and severity of cardiac dysfunction and clinical disease. Several aspects of CNH assays are still to be elucidated, and further work is needed to

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“…ACE activity was estimated by measuring the hydrolysis of 100 fimo\/L [glycine-l- 14 C]hippuryl-L-histidyl-Lleucine (3 mCi/mmol, Amersham) in the presence or absence of 10~7 mol/L captopril. Incubations (final volume, 100 /u.L) were performed at 37°C under conditions of initial velocity measurement in 0.1 mol/L phosphate buffer, pH 8.0, containing 0.3 mol/L NaCl and 10 /xmol/L ZnCl 2 and were stopped after 5 hours by adding 50 fiL 0.3N HC1, as described by Cushman and Cheung.…”

Section: Determination Of Plasma and Cardiac Angiotensin Converting Ementioning

confidence: 99%

“…20 14 C metabolites were separated from the substrate by adding 0.5 mL ethyl acetate to the acidified enzyme reaction mixture and shaking for 1 minute. The mixture was centrifuged at 18 000g for 7 minutes, and a 0.3-mL aliquot of the organic layer containing 14 C metabolites was counted by scintillation spectrometry (Pico-Fluor 15, Packard Instrument Co). Contamination by the substrate was less than 3%, and the metabolite recovery was more than 90%.…”

Section: Determination Of Plasma and Cardiac Angiotensin Converting Ementioning

confidence: 99%

“…A inhibitor of nitric oxide synthase in vitro, 14 /V G -nitro-L-arginine-methyl ester (L-NAME) also inhibits the release of nitric oxide from endothelial cells and aortic rings. In vivo L-NAME administration to rodents is accompanied by a rise in blood pressure and a generalized decrease in peripheral blood flow, indicating that a continuous release of nitric oxide actively maintains vasodilator tone.…”

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Cardiac weight in hypertension induced by nitric oxide synthase blockade.

et al. 1993

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Wistar rats given a nitric oxide synthase inhibitor, iV c -nitro-L-arginine-methyl ester (L-NAME), for 4 weeks develop time-and dose-dependent hypertension without cardiac hypertrophy. This initial study of the relation between left ventricular weight and L-NAME-induced hypertension has now been extended by giving 50 mg/kg per day L-NAME to Wistar rats (n=30) for 8 weeks and comparing results with those from control rats (n=10) and two-kidney, one clip rats (n=14). Although L-NAME rats and two-kidney, one clip rats had increased systolic blood pressures during the last 3 weeks of the experiment (202 ±24 and 224±16 mm Hg, respectively), the ratio of left ventricular weight to body weight of L-NAME rats (2.12±0.32 mg/g) was not statistically different from that of control rats (1.93±0.13 mg/g), whereas that of two-kidney, one clip rats was increased (2.85 ±0.20 mg/g). The plasma renin activity of L-NAME rats was not significantly different from that of control rats. Two L-NAME rat subgroups were defined according to the presence of left ventricular hypertrophy (ratio of left ventricular weight to body weight >2.19 mg/g, control mean+2 SD) (6 of 25) or its absence (19 of 25). Systolic blood pressure, plasma renin activity, and cardiac angiotensin converting enzyme activity of L-NAME rats with left ventricular hypertrophy were significantly higher than those of the subgroup without. In a multiple regression analysis using the ratio of left ventricular weight to body weight as an independent variable and three dependent variables (L-NAME administration, plasma renin activity, and systolic blood pressure), we found that all of these three variables contributed to left ventricular weight independently of each other. Thus, even if the degree of left ventricular hypertrophy evolves in parallel with the duration and magnitude of a chronic rise in blood pressure, other factors, such as the renin-angiotensin system and nitric oxide production, influence this relation. (Hypertension. 1993;22:380-387.) KEY WORDS • guanosine cyclic monophosphate • heart hypertrophy • nitric oxide • renin A inhibitor of nitric oxide synthase in vitro, 14 /V G -nitro-L-arginine-methyl ester (L-NAME) also inhibits the release of nitric oxide from endothelial cells and aortic rings. In vivo L-NAME administration to rodents is accompanied by a rise in blood pressure and a generalized decrease in peripheral blood flow, indicating that a continuous release of nitric oxide actively maintains vasodilator tone. 2 ' 5 Rats given L-NAME for 4 weeks show a time-and dose-dependent increase in blood pressure. 6 -7 Surprisingly, in our hypertensive rats, the total ratio of heart weight to body weight did not increase after 4 weeks of L-NAME administration (1 to 100 mg/kg per day). 6 This absence of hypertrophy was in contrast to results obtained in the other models of experimental hypertension in which a chronic increase in blood pressure was accompanied by cardiac hypertrophy. 812 This study of the relation between heart weight and L-NAME-induced hypert...

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Effects of propranolol and pindolol on plasma ANP levels in humans at rest and during exercise

Cited by 14 publications

References 0 publications

Introduction of Metoprolol Increases Plasma B-Type Cardiac Natriuretic Peptides in Mild, Stable Heart Failure

Introduction of Metoprolol Increases Plasma B-Type Cardiac Natriuretic Peptides in Mild, Stable Heart Failure

Diagnostic Accuracy and Prognostic Relevance of the Measurement of Cardiac Natriuretic Peptides: A Review

Cardiac weight in hypertension induced by nitric oxide synthase blockade.

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