Bovine atrial natriuretic peptide in heart failure

ABSTRACT The present study describes the concentration and molecular form of atrial natriuretic peptide (ANP) in Holstein dairy cattle with mild (bacterial endocarditis; BEC) or severe (dilated cardiomyopathy; DCM) heart failure. Significant increases in plasma concentration of ANP were observed in cattle with DCM (73·3 ± 16·02 pmol/l, n=4, P<0·01) and BEC (20·6± 3·45 pmol/l, n=7, P<0·05), when compared with those in control cattle (14·5± 1·84 pmol/l, n= 12). The concentration of ANP in cattle with DCM was significantly (P<0·01) higher compared with that in cattle with BEC. Plasma concentration of ANP correlated significantly with right atrial pressure (r =0·95, P<0·01) and left ventricular end-diastolic pressure (r= 0·84, P<0·01). Gel-permeation chromatography of ANP in plasma and the right atrium from control and cattle with BEC revealed a single peak corresponding to the elution position of authentic human ANP(99–126) in plasma, and two peaks corresponding to those of authentic human ANP(99–126) and pro-ANP in the atrial extract. In cattle with DCM, however, peaks corresponding to the elution positions of authentic human β-ANP and/or pro-ANP were detected in addition to the peak corresponding to ANP(99–126). The content of ANP in the right atrium of cattle with DCM was significantly (P<0·05) increased compared with that in control cattle and those with BEC. The present study therefore suggests that the synthesis and secretion of ANP might be stimulated by atrial distention induced by increased atrial pressure. This suggestion is supported by the fact that the middle molecular weight form of ANP, possibly corresponding to human β-ANP, was detected in both the plasma and atria of the cattle with severe heart failure. Journal of Endocrinology (1990) 124, 463–467

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The effect of short-lasting atrial pacing on the release of atrial natriuretic peptide, vasopressin, and methionine enkephalin in man

Acta Endocrinologica ◽

10.1530/acta.0.1160235 ◽

1987 ◽

Vol 116 (2) ◽

pp. 235-240 ◽

Cited By ~ 4

Author(s):

Kozo Ota ◽

Tokihisa Kimura ◽

Meiichi Ito ◽

Minoru Inoue ◽

Masaru Shoji ◽

...

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Atrial Pressure ◽

Right Atrial ◽

Right Atrial Pressure ◽

Atrial Pacing ◽

Methionine Enkephalin ◽

Arterial Blood ◽

The Right ◽

Atrial Natriuretic

Abstract. In order to study the effect of atrial tachycardia on the release of atrial natriuretic peptide (ANP), AVP, and methionine enkephalin (M-Enk), plasma concentrations of these peptides in the right ventricle were determined in patients with various arrhythmias (N = 10) during cardiac catheterization and incremental atrial pacing. Each pacing (100 per min, the maximum rate for 1:1 atrioventricular conduction, and 200 per min) lasted 4 to 5 min. Plasma ANP was significantly increased from 53.1 ± 12.2 in the resting condition to 168.9 ± 59.9 pmol/l at a pacing rate of 200 beats per min (P < 0.05); plasma AVP tended to decrease, but not significantly, and plasma M-Enk did not change at all. Pulse pressure in the right atrium (PPRA) and mean right atrial pressure (MRAP) tended to increase during the pacing, and at the rate of 200 beats per min PPRA was significantly higher than at the rate of 100 beats per min. Mean arterial blood pressure, plasma osmolality, and plasma sodium and potassium concentrations did not change significantly. There were significant correlations between plasma ANP and PPRA, MRAP and heart rate. These results indicate that atrial pacing stimulates ANP release with a rise in right atrial pressure, but does not influence M-Enk and AVP releases.

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Haemodynamic and Hormonal Responses to Cardiac Pacing in Humans: Influence of Different Stimulation Sequences and Rates

Clinical Science ◽

10.1042/cs0880165 ◽

1995 ◽

Vol 88 (2) ◽

pp. 165-172 ◽

Cited By ~ 4

Author(s):

Hans Berglund ◽

Anders Edlund ◽

Elvar Theodorsson ◽

Hans Vallin

Keyword(s):

Plasma Concentration ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Atrial Pressure ◽

Right Atrial ◽

Pulmonary Capillary ◽

Peptide Release ◽

Arterial Plasma ◽

Wedge Pressure ◽

Atrial Natriuretic

1. To examine the effects of rate and pressure on release of vasoactive hormones, 10 healthy subjects were examined. 2. A standardized pacing protocol was used to achieve different haemodynamic responses at two predetermined heart rates. Haemodynamic variables, and plasma concentrations of atrial natriuretic peptide, arginine vasopressin, adrenaline and noradrenaline were measured. 3. Right atrioventricular pacing at a rate of 150 impulses/min resulted in disparate responses in right atrial pressure (slight decrease) and pulmonary capillary wedge pressure (increase). Change in arterial plasma concentration of atrial natriuretic peptide correlated to change in pulmonary capillary wedge pressure, and change in arterial plasma concentration of noradrenaline correlated to change in total systemic vascular resistance, whereas concentrations of adrenaline and arginine vasopressin did not alter significantly during the stimulation periods. A significant influence of rate in addition to the pressure related influence on plasma concentration of atrial natriuretic peptide was found. In contrast, an increase in rate in the absence of an increase in atrial pressures did not raise the plasma concentration of atrial natriuretic peptide. There was no significant relationship between change in atrial natriuretic peptide and noradrenaline. 4. These data support the concept of a rate dependence of atrial natriuretic peptide release in man. Increased atrial pressure and thus presumed atrial stretch seems to be a prerequisite for increased plasma concentration of atrial natriuretic peptide. In addition, these results highlight the importance of monitoring both left and right atrial pressure in clinical investigations assessing modulation of atrial natriuretic peptide release.

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Relationship between plasma atrial natriuretic peptide concentration and atrial pressure in acute and chronic heart failure.

Japanese Heart Journal ◽

10.1536/ihj.31.425 ◽

1990 ◽

Vol 31 (4) ◽

pp. 425-434 ◽

Cited By ~ 4

Author(s):

Motoyuki NAKAMURA ◽

Naoshi ARAKAWA ◽

Yasumi ABE ◽

Hiroaki YOSHIDA ◽

Shuetsu MIURA ◽

...

Keyword(s):

Heart Failure ◽

Chronic Heart Failure ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Atrial Pressure ◽

Plasma Atrial Natriuretic Peptide ◽

Peptide Concentration ◽

Atrial Natriuretic

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N-Terminal Pro–Atrial Natriuretic Peptide Measurement in Plasma Suggests Covalent Modification

Clinical Chemistry ◽

10.1373/clinchem.2011.166330 ◽

2011 ◽

Vol 57 (9) ◽

pp. 1327-1330 ◽

Cited By ~ 33

Author(s):

Ingrid Hunter ◽

Urban Alehagen ◽

Ulf Dahlström ◽

Jens F Rehfeld ◽

Dan L Crimmins ◽

...

Keyword(s):

Heart Failure ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Clinical Performance ◽

Roc Curves ◽

Healthcare Setting ◽

Left Ventricular ◽

Covalent Modification ◽

Moderate Heart Failure ◽

Atrial Natriuretic

BACKGROUND The N-terminal fragment of cardiac-derived pro–B-type natriuretic peptide is a glycosylated polypeptide. It is unknown whether N-terminal pro–atrial natriuretic peptide (proANP) fragments are also covalently modified. We therefore evaluated the clinical performance of 2 distinctly different proANP assays on clinical outcome. METHODS We examined 474 elderly patients with symptoms of heart failure presenting in a primary healthcare setting. Samples were analyzed with an automated immunoluminometric midregion proANP (MR-proANP) assay and a new processing-independent assay (PIA) developed in our laboratory. The results were compared with Bland–Altman plots, and clinical performance was assessed by generating ROC curves for different clinical outcomes. RESULTS Despite linear regression results indicating a good correlation (r = 0.85; P < 0.0001), the PIA measured considerably more proANP than the MR-proANP assay (mean difference, 663 pmol/L; SD, 478 pmol/L). In contrast, the clinical performances of the 2 assays [as assessed by the area under the ROC curve (AUC)] in detecting left ventricular dysfunction were similar [proANP PIA, 0.71 (95% CI, 0.63–0.79); MR-proANP assay, 0.74 (95% CI, 0.66–0.81); P = 0.32]. The prognostic ability to report cardiovascular mortality during a 10-year follow-up revealed AUC values of 0.66 (95% CI, 0.60–0.71) for the proANP PIA and 0.69 (95% CI, 0.63–0.74) for the MR-proANP assay (P = 0.08, for comparing the 2 assays). CONCLUSIONS Our data suggest that N-terminal proANP fragments in patient plasma differ from the calibrator peptides used but that the difference does not affect ROC curves in an elderly cohort of patients with mild to moderate heart failure. We suggest that human N-terminal proANP fragments can be covalently modified.

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Role of endogenous atrial natriuretic peptide on systemic and renal hemodynamics in heart failure rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.1.h182 ◽

1994 ◽

Vol 267 (1) ◽

pp. H182-H186 ◽

Cited By ~ 3

Author(s):

T. Nishikimi ◽

K. Miura ◽

N. Minamino ◽

K. Takeuchi ◽

T. Takeda

Keyword(s):

Heart Failure ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Diastolic Pressure ◽

Urinary Sodium Excretion ◽

Left Ventricular ◽

Renal Hemodynamics ◽

Renal Tubular ◽

Atrial Natriuretic

To investigate the role of endogenous atrial natriuretic peptide (ANP) in rats with heart failure (HF), we administered HS-142-1 (HS; 3 mg/kg body wt iv), a novel nonpeptide ANP-receptor antagonist, to rats with surgically induced myocardial infarction and sham-operated rats. HF was characterized by a higher left ventricular end-diastolic pressure and higher plasma ANP concentration vs. controls. HS administration significantly reduced the plasma and urinary levels of guanosine 3',5'-cyclic monophosphate in rats with HF [plasma concentration 10.6 +/- 2.6 vs. 2.7 +/- 0.4 nM (P < 0.05); urinary excretion 48 +/- 8 vs. 12 +/- 2 pmol/min (P < 0.05)]. Systemic and renal hemodynamics were unaffected by HS administration. Urine flow (-35%) and urinary sodium excretion (-50%) were significantly decreased after HS only in those rats with HF that had no changes in systemic and renal hemodynamics. These results suggest that the elevated ANP levels in HF do not contribute directly to the maintenance of systemic hemodynamics but rather compensate for the HF mainly via diuresis and natriuresis, achieved by the inhibition of renal tubular reabsorption rather than by renal vasodilatation.

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Atrial natriuretic peptide and sodium homeostasis in compensated heart failure

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1996.271.5.r1353 ◽

1996 ◽

Vol 271 (5) ◽

pp. R1353-R1363 ◽

Cited By ~ 2

Author(s):

T. E. Lohmeier ◽

H. L. Mizelle ◽

G. A. Reinhart ◽

J. P. Montani ◽

C. E. Hord ◽

...

Keyword(s):

Heart Failure ◽

Cardiac Output ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Plasma Levels ◽

Left Ventricular ◽

Sodium Balance ◽

Plasma Norepinephrine ◽

Norepinephrine Concentration ◽

Atrial Natriuretic

The purpose of this study was to determine whether high plasma levels of atrial natriuretic peptide (ANP) in compensated heart failure are important in the maintenance of sodium balance. This was achieved by subjecting eight dogs to bilateral atrial appendectomy (APX) to blunt the ANP response to pacing-induced heart failure. Five intact dogs served as controls. In controls, 14 days of left ventricular pacing at 240 beats/min produced a sustained fall in cardiac output and mean arterial pressure of approximately 40 and 20%, respectively; compared with cardiac output, reductions in renal blood flow (up to approximately 25%) were less pronounced and even smaller decrements in GFR occurred (up to 9%). Despite these changes and a threefold elevation in plasma norepinephrine concentration, plasma renin activity (PRA) did not increase and sodium balance was achieved during the second week of pacing in association with a six- to eightfold rise in plasma levels of ANP. Similar responses occurred in four dogs in which APX was relatively ineffective in blunting the ANP response to pacing. In marked contrast, there were substantial increments in PRA and in plasma norepinephrine concentration, and marked sodium and water retention during the last week of pacing in four dogs with APX and severely deficient ANP. These results indicate that ANP plays a critical role in promoting sodium excretion in the early stages of cardiac dysfunction.

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Mechanism for decrease in cardiac output with atrial natriuretic peptide in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.256.3.h760 ◽

1989 ◽

Vol 256 (3) ◽

pp. H760-H765 ◽

Cited By ~ 8

Author(s):

R. W. Lee ◽

S. Goldman

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Blood Volume ◽

Left Ventricular ◽

Right Atrial ◽

Total Blood Volume ◽

Total Blood ◽

Atrial Natriuretic

To examine the mechanism by which atrial natriuretic peptide (ANP) decreases cardiac output, we studied changes in the heart, peripheral circulation, and blood flow distribution in eight dogs. ANP was given as a bolus (3.0 micrograms/kg) followed by an infusion of 0.3 microgram.kg-1.min-1. ANP did not change heart rate, total peripheral vascular resistance, and the first derivative of left ventricular pressure but decreased mean aortic pressure from 91 +/- 4 to 76 +/- 3 mmHg (P less than 0.001) and cardiac output from 153 +/- 15 to 130 +/- 9 ml.kg-1.min-1 (P less than 0.02). Right atrial pressure and left ventricular end-diastolic pressure also decreased. Mean circulatory filling pressure decreased from 7.1 +/- 0.3 to 6.0 +/- 0.3 mmHg (P less than 0.001), but venous compliance and unstressed vascular volume did not change. Resistance to venous return increased from 0.056 +/- 0.008 to 0.063 +/- 0.010 mmHg.ml-1.kg.min (P less than 0.05). Arterial compliance increased from 0.060 +/- 0.003 to 0.072 +/- 0.004 ml.mmHg-1.kg-1 (P less than 0.02). Total blood volume and central blood volume decreased from 82.2 +/- 3.1 to 76.2 +/- 4.6 and from 19.8 +/- 0.8 to 17.6 +/- 0.6 ml/kg (P less than 0.02), respectively. Blood flow increased to the kidneys. We conclude that ANP decreases cardiac output by decreasing total blood volume. This results in a lower operating pressure and volume in the venous capacitance system with no significant venodilating effects. Cardiac factors and a redistribution of flow to the splanchnic organs are not important mechanisms to explain the decrease in cardiac output with ANP.

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