Atrial Natriuretic Peptide Elevation in Congestive Heart Failure in the Human

Burnett, J. C.; Kao, Pai C.; Hu, DC; Heser, DW; Heublein, Denise M.; Granger, J. P.; Opgenorth, T J; Reeder, G. S.

doi:10.1126/science.2935937

Cited by 867 publications

(322 citation statements)

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“…Increases in proteinuria and circulating levels of ANP have been positively correlated with the severity of HF in human HF (1,5,6,25) and in this model (32,33) of HF. Importantly, our exercise intervention slowed the age-related increase in plasma ANP as indicated by our observation that TR animals displayed significantly less ANP over time than their sedentary counterparts after 6 mo of training.…”

Section: Discussionmentioning

confidence: 99%

Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats

Emter

McCune²,

Sparagna³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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. Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats. Am J Physiol Heart Circ Physiol 289: H2030 -H2038, 2005. First published July 1, 2005; doi:10.1152/ajpheart.00526.2005.-Data regarding the effectiveness of chronic exercise training in improving survival in patients with congestive heart failure (CHF) are inconclusive. Therefore, we conducted a study to determine the effect of exercise training on survival in a well-defined animal model of heart failure (HF), using the lean male spontaneously hypertensive HF (SHHF) rat. In this model, animals typically present with decompensated, dilated HF between ϳ18 and 23 mo of age. SHHF rats were assigned to sedentary or exercise-trained groups at 9 and 16 mo of age. Exercise training consisted of 6 mo of low-intensity treadmill running. Exercise training delayed the onset of overt HF and improved survival (P Ͻ 0.01), independent of any effects on the hypertensive status of the rats. Training delayed the myosin heavy chain (MyHC) isoform shift from ␣-to ␤-MyHC that was seen in sedentary animals that developed HF. Exercise was associated with a concurrent increase in cardiomyocyte length (Ϸ6%), width, and area and prevented the increase in the length-to-width ratio seen in sedentary animals in HF. The increases in proteinuria, plasma atrial natriuretic peptide, and serum leptin levels observed in rats with HF were suppressed by low-intensity exercise training. No significant alterations in sarco (endo)plasmic reticulum Ca 2ϩ ATPase, phospholamban, or Na ϩ / Ca 2ϩ exchanger protein expression were found in response to training. Our results indicate that 6 mo of low-intensity exercise training delays the onset of decompensated HF and improves survival in the male SHHF rat. Similarly, exercise intervention prevented or suppressed alterations in several key variables that normally occur with the development of overt CHF. These data support the idea that exercise may be a useful and inexpensive intervention in the treatment of HF. myosin heavy chain; proteinuria; cardiomyocyte morphology; atrial natriuretic peptide; leptin HEART DISEASE is a leading cause of death among men and women in Western industrialized societies. Cardiovascular disease (CVD) currently affects over 70 million Americans, 65 million of which are estimated to have high blood pressure and nearly 5 million are diagnosed with congestive heart failure (CHF) (2). With the diagnosis of CHF, life expectancy decreases dramatically and chances of survival decrease with 70 -80% of patients dying within 8 yr (2). Although chronic exercise training has clearly been shown to be beneficial in attenuating risk factors for CVD, including high blood pressure and cholesterol levels, insulin resistance, and obesity (9,14,53,58), the utility of exercise as a clinical intervention for patients with developing CHF is less clear. Currently, there is a lack of clarity regarding the efficacy of chronic exercise training as a treatment and in reducing mortali...

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Section: Discussionmentioning

confidence: 99%

Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats

Emter

McCune²,

Sparagna³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…Pulmonary capillary wedge pressure, pulmonary arterial pressure, and right atrial pressure were determined with a Swan-Ganz catheter ( Measurements of the plasma hormones. The plasma ANP concentration was measured by a specific RIA for a-ANP reported previously.9 31 32 Briefly, this RIA recognizes a carboxyterminal fragment of ANP, a-ANP (17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28), and the minimal detectable quantity of a-human ANP is 1 pg/tube. Plasma renin activity and the plasma aldosterone concentration were measured with commercially available kits, Renin RIA beads (Dainabot Co., Ltd., Tokyo, Japan) and Aldosterone Test Shionogi (Shionogi Co., Ltd., Osaka, Japan), which are based on previously reported methods.33 3 Plasma norepinephrine and epinephrine levels were measured by high-performance liquid chromatography combined with the trihydroxyindole fluorometric procedure.…”

Section: Methodsmentioning

confidence: 99%

Clinical application of atrial natriuretic polypeptide in patients with congestive heart failure: beneficial effects on left ventricular function.

Saito¹,

Nakao²,

Nishimura³

et al. 1987

Circulation

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167

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Synthetic a-human atrial natriuretic polypeptide was infused in patients with congestive heart failure (CHF) (New York Heart Association class III or IV) and in those without CHF. The infusion of atrial natriuretic polypeptide (ANP) at a rate of 0. 1 gg/kg/min significantly decreased pulmonary capillary wedge pressure and increased stroke volume index in all of the patients with CHF, whereas it decreased pulmonary capillary wedge pressure but caused no significant change in stroke volume index in the patients without CHF. Concomitant significant reductions in total systemic resistance were observed in both groups of patients. The ANP infusion significantly increased the urine volume, the excretion of sodium, and endogenous creatinine clearance in the patients without CHF. In the patients with CHF, it also showed a tendency to increase all these variables, but the urine volume did not correlate with the reduction in pulmonary capillary wedge pressure. The ANP infusion also decreased plasma aldosterone concentrations in these patients, although no significant difference was observed in the decrement of the plasma aldosterone concentration in the patients with and those without CHF. These findings indicate that the ANP infusion improves left ventricular function in patients with CHF, and suggest that this improvement results mainly from the vasodilating activity of ANP.Circulation 76, No. 1, 115-124, 1987. AFTER THE EPOCHAL discovery of the potent diuretic, natriuretic, and vasorelaxant activities in an extract from rat atria by de Bold et al. ,' multiple forms of natriuretic polypeptides with high and low molecular weights have been isolated fromn rat and human atria and implicated in the control of blood pressure, water, and electrolyte balance.2-1 Accumulating evidence indicates that a-atrial natriuretic polypeptide (a-ANP)

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“…[1][2][3][4][5][6][7] BNP is secreted from the failing heart into the systemic circulation; the plasma level of this peptide is elevated in patients with heart failure. 8 -11 The plasma BNP level has been recognized as a biochemical marker of ventricular dysfunction.…”

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confidence: 99%

Plasma Level of B-Type Natriuretic Peptide as a Prognostic Marker After Acute Myocardial Infarction

et al. 2004

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Background-Circulating levels of B-type natriuretic peptide (BNP), a cardiac hormone, reflect the severity of cardiac dysfunction. Because the plasma BNP level changes dramatically during the period after the onset of acute myocardial infarction (AMI), identification of a suitable sampling time is problematic. There have been several reports indicating that the plasma BNP level obtained in the acute phase of AMI can be used as a prognostic marker. We examined whether the plasma BNP level measured 3 to 4 weeks after the onset of AMI represents a reliable prognostic marker for patients with AMI. Methods and Results-We analyzed 145 consecutive patients with AMI. Plasma BNP levels were measured during the 3 to 4 weeks after onset of AMI. Of those patients, 23 experienced fatal cardiac events during this study. The mean follow-up period was 58.6 months. Log BNP, left ventricular end-diastolic pressure, and pulmonary vascular resistance were all significantly higher in the cardiac death group, and there were more men and more patients with a history of heart failure in the cardiac death group. A Cox proportional hazards model analysis showed that log BNP was an independent predictor of cardiac death. The survival rate was significantly higher in patients with log BNP Ͻ2.26 (180 pg/mL) than in those with log BNP Ն2.26. Conclusions-The plasma BNP level obtained 3 to 4 weeks after the onset of AMI can be used as an independent predictor of cardiac death in patients with AMI.

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Atrial Natriuretic Peptide Elevation in Congestive Heart Failure in the Human

Cited by 867 publications

References 10 publications

Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats

Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats

Clinical application of atrial natriuretic polypeptide in patients with congestive heart failure: beneficial effects on left ventricular function.

Plasma Level of B-Type Natriuretic Peptide as a Prognostic Marker After Acute Myocardial Infarction

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