Plasma Concentrations and Comparisons of Brain Natriuretic Peptide and Atrial Natriuretic Peptide in Normal Subjects and Patients with Essential Hypertension

AbstractWe evaluated the analytical performance of a fully-automated electrochemiluminescence “sandwich” immunoassay method for the N-terminal fragment of the pro-peptide of brain natriuretic peptide (BNP). We then compared the diagnostic accuracy of this method in discriminating between normal subjects and patients with cardiomyopathy with that found with two previously described immunoradiometric assay methods for the assay of atrial natriuretic peptide (ANP) and BNP. We studied 193 consecutive patients (mean age 64.4±12.3 years, range 20–89 years, including 56 women and 137 men) with chronic cardiomyopathy and a group of 85 healthy subjects (mean age 52.3±12.0 years, 42 women and 43 men, range 20–79 years). N-terminal fragment of proBNP

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Comparative Effects of Atrial Natriuretic Peptide and Brain Natriuretic Peptide on the Aldosterone and Pressor Responses to Angiotensin Ii in Man

Clinical Science ◽

10.1042/cs0880081 ◽

1995 ◽

Vol 88 (1) ◽

pp. 81-86 ◽

Cited By ~ 11

Author(s):

Robert I. Cargill ◽

Allan D. Struthers ◽

Brian J. Lipworth

Keyword(s):

Steady State ◽

Angiotensin Ii ◽

Atrial Natriuretic Peptide ◽

Brain Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Concentrations ◽

Plasma Aldosterone ◽

Renin Angiotensin Aldosterone System ◽

Renin Angiotensin ◽

Atrial Natriuretic

1. Atrial natriuretic peptide and brain natriuretic peptide have similar vasodilator and natriuretic properties, although little information is available regarding their relative effects as antagonists of the renin—angiotensin—aldosterone system. We have therefore compared how atrial natriuretic peptide and brain natriuretic peptide affect the systemic pressor and aldosterone responses to angiotensin II in eight male subjects. 2. Each subject was studied on three separate occasions, when they received a 60-min infusion of placebo, atrial natriuretic peptide (10 pmol min−1 kg−1) or brain natriuretic peptide (10 pmolmin−1 kg−1), with a concomitant infusion of angiotensin II (6 ng min−1 kg−1) given for the final 30 min of the infusion period. The change in haemodynamic parameters and plasma aldosterone induced by angiotensin II was measured. Plasma concentrations of atrial natriuretic peptide (182 ± 23 pmol/l) and brain natriuretic peptide (193 ± 25 pmol/l) achieved at steady-state during the infusion on each study day were not significantly different. 3. Increases in mean arterial pressure in response to angiotensin II were significantly lowered by concomitant infusion of atrial natriuretic peptide (21.0 ± 1.7 mmHg) and brain natriuretic peptide (20.1 ± 1.9 mmHg) compared with placebo (29.0 ± 4.1 mmHg). There were similar effects on systolic and diastolic blood pressure. Cardiac output was decreased on each study day to the same extent by angiotensin II infusion. Total systemic vascular resistance showed a non-significant trend towards an attenuated response to angiotensin II when atrial natriuretic peptide or brain natriuretic peptide was infused concomitantly in comparison with placebo. 4. Plasma aldosterone increased by 326 ± 49 pmol/l when angiotensin II was infused with placebo. Both atrial natriuretic peptide and brain natriuretic peptide significantly blunted this response, although the increase with atrial natriuretic peptide (19 ± 35 pmol/l) was significantly lower than the increase with brain natriuretic peptide (133 ± 19 pmol/l). 5. Atrial natriuretic peptide and brain natriuretic peptide were therefore equally effective in blunting the systemic pressor response to angiotensin II. It was apparent, however, in view of similar plasma concentrations at steady state, that on a molar basis atrial natriuretic peptide was a more potent inhibitor of angiotensin II-induced aldosterone secretion than brain natriuretic peptide. These results suggest a dissociation between the haemodynamic and hormonal effects of atrial natriuretic peptide and brain natriuretic peptide in terms of antagonism of the renin—angiotensin—aldosterone system.

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Effects of Calcium Antagonists and Nitroglycerin on Atrial Natriuretic Peptide in Normal Subjects and Patients with Essential Hypertension

Angiology ◽

10.1177/000331978904000105 ◽

1989 ◽

Vol 40 (1) ◽

pp. 24-28 ◽

Cited By ~ 11

Author(s):

Tsutomu Iwasaki ◽

Akihiro Niwa ◽

Toshio Shinoda ◽

Masaki Ishihara ◽

Toru Aizawa ◽

...

Keyword(s):

Essential Hypertension ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Calcium Antagonists ◽

Normal Subjects ◽

Atrial Natriuretic

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Pulsatile secretion of atrial natriuretic peptide and brain natriuretic peptide in healthy humans

Clinical Science ◽

10.1042/cs0970201 ◽

1999 ◽

Vol 97 (2) ◽

pp. 201-206 ◽

Cited By ~ 18

Author(s):

Erling B. PEDERSEN ◽

Henrik B. PEDERSEN ◽

Kaare T. JENSEN

Keyword(s):

Heart Failure ◽

Atrial Natriuretic Peptide ◽

Brain Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Concentrations ◽

Blood Samples ◽

Pulsatile Secretion ◽

Healthy Humans ◽

Severity Of The Disease ◽

Atrial Natriuretic

Both atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are involved in sodium and water homoeostasis in healthy humans. The plasma concentrations of the natriuretic peptides can be used to differentiate between dyspnoea of cardiac and pulmonary origin, and the degree of elevation of the peptide levels in the plasma in heart failure is a measure of the severity of the disease. However, the patterns of secretion of ANP and BNP are not clear either in healthy humans or in patients. The purpose of the present study was to test the hypotheses that both ANP and BNP are secreted in pulses in healthy humans, and that this phenomenon can be revealed by determination of ANP and BNP in peripheral venous blood samples. In 12 healthy subjects, blood samples were drawn every 2 min through an intravenously inserted plastic needle over a period of 2 h. Plasma concentrations of ANP and BNP were determined by RIAs, and the results were analysed for pulsatile behaviour by Fourier transformation. Pulsatile secretion of ANP was seen in 10 out of 12 subjects [ν = 0.028 min-1 (median; range 0.013–0.047 min-1), i.e. a pulse of ANP with an interval of 36 min (range 21–77 min)]. Pulsatile secretion of BNP was seen in nine out of 12 patients [ν = 0.021 min-1 (range 0.013–0.042 min-1), i.e. a pulse of BNP with an interval of 48 min (range 24–77 min)]. The main conclusion is that the secretion patterns of both ANP and BNP are pulsatile in most healthy humans. Consequently, it is important to study whether pulsatile secretion also occurs in heart failure in order to obtain the most informative predictive values both in the differential diagnosis of dyspnoea and in the evaluation of the severity of the disease.

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Elevated Plasma C-Type Natriuretic Peptide Concentrations in Patients with Chronic Renal Failure

Clinical Science ◽

10.1042/cs0870319 ◽

1994 ◽

Vol 87 (3) ◽

pp. 319-322 ◽

Cited By ~ 35

Author(s):

Kazuhito Totsune ◽

Kazuhiro Takahashi ◽

Osamu Murakami ◽

Fumitoshi Satoh ◽

Masahiko Sone ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Renal Failure ◽

Chronic Renal Failure ◽

Atrial Natriuretic Peptide ◽

Brain Natriuretic Peptide ◽

Natriuretic Peptide ◽

Heart Association ◽

Normal Subjects ◽

Atrial Natriuretic

1. C-type natriuretic peptide is a neuropeptide, which is also produced by the vascular endothelial cells. Plasma immunoreactive C-type natriuretic peptide concentrations in patients with various diseases have not yet been studied. 2. Plasma immunoreactive C-type natriuretic peptide concentrations were studied by radioimmunoassay in normal subjects, patients with congestive heart failure, non-dialysed patients with chronic renal failure and haemodialysis patients with chronic renal failure. The C-type natriuretic peptide levels were compared with the levels of atrial natriuretic peptide and brain natriuretic peptide. 3. Plasma immunoreactive C-type natriuretic peptide concentrations were greatly elevated in patients with chronic renal failure [non-dialysed, 13.0 ± 4.2 pmol/l (mean ± SEM), n = 9, P < 0.01) compared with normal subjects (4.4 ± 0.4 pmol/l, n = 26); haemodialysis, 16.1 ± 2.1 pmol/l, n = 13, P < 0.01], but not in patients with congestive heart failure (New York Heart Association Class II-IV, 3.0 ± 0.7 pmol/l, n = 11, P > 0.05). Plasma immunoreactive atrial natriuretic peptide and brain natriuretic peptide concentrations were elevated both in patients with congestive heart failure and in haemodialysis patients with chronic renal failure. 4. Reverse-phase high performance liquid chromatography showed that immunoreactive C-type natriuretic peptide in plasma from normal subjects and haemodialysis patients was eluted in the positions of C-type natriuretic peptide −22 and −53. 5. These findings suggest that C-type natriuretic peptide is a non-cardiac circulating hormone and participates in the cardiovascular regulation in a different manner from atrial natriuretic peptide and brain natriuretic peptide.

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Atrial natriuretic peptide: Evidence of action as a natriuretic hormone at physiological plasma concentrations in man

Clinical Science ◽

10.1042/cs0720305 ◽

1987 ◽

Vol 72 (3) ◽

pp. 305-312 ◽

Cited By ~ 106

Author(s):

J. V. Anderson ◽

J. Donckier ◽

N. N. Payne ◽

J. Beacham ◽

J. D. H. Slater ◽

...

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Concentrations ◽

Plasma Renin ◽

Normal Subjects ◽

Natriuretic Hormone ◽

Plasma Aldosterone Concentration ◽

Water Excretion ◽

Physiological Range ◽

Atrial Natriuretic

1. The administration of exogenous atrial natriuretic peptide (ANP) causes a natriuresis and diuresis in man, but this has, to date, only been demonstrated at plasma ANP concentrations within the high pathological or pharmacological ranges. Evidence that ANP acts physiologically requires the demonstration of a natriuretic effect when it is infused to recreate plasma concentrations similar to those observed after physiological stimuli. 2. We infused human α-ANP (1–28) at a calculated rate of 1.2 pmol min−1 kg−1 for 3 h into seven water-loaded normal subjects, achieving plasma ANP concentrations within the upper part of the physiological range. The subjects' resting plasma ANP concentration increased from 3.8 ± 1.5 to 20.9 ± 1.9 pmol/l. 3. The infusion of ANP caused a 60% increase of mean urinary sodium excretion from 111 ± 18 to 182 ± 30 μmol/min (P < 0.001) and a 28% increase of mean water excretion from 10.8 ± 0.8 to 13.8 ± 1.6 ml/min (P < 0.01). 4. The infusion suppressed mean plasma renin activity from 1.55 ± 0.10 to 1.17 ± 0.06 pmol of ANG I h−1 ml−1 (P < 0.001). Mean plasma aldosterone concentration (242 ± 16 basally and 215 ± 15 pmol/l at the end of ANP infusion) did not change significantly. Pulse rate and blood pressure were unchanged throughout the study. 5. No significant change in any of the variables mentioned above occurred during the infusion of the vehicle alone on a separate study day. 6. The demonstration that recreation of plasma concentrations of ANP within the physiological range by intravenous infusion induces a natriuresis provides new evidence supporting the role of ANP as a natriuretic hormone.

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