Atrial natriuretic peptide in heart failure

Brandt, Roland R.; Wright, R. Scott; Redfield, Margaret M.; Burnett, John C.

doi:10.1016/0735-1097(93)90468-g

Cited by 82 publications

(44 citation statements)

References 38 publications

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“…Increased circulating levels of ANF have been positively correlated with the severity of heart failure. 37,38 Importantly, our swimming protocol reduced the expression of ANF, at least at the mRNA level, as indicated by the real-time RT-PCR experiments, supporting the idea that endurance training impacts beneficially on cardiac performance, even in the presence of pathological CH.…”

Section: Discussionmentioning

confidence: 55%

Endurance Training in the Spontaneously Hypertensive Rat

et al. 2009

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Abstract-The effect of endurance training (swimming 90 min/d for 5 days a week for 60 days) on cardiac hypertrophy was investigated in the spontaneously hypertensive rat (SHR). Sedentary SHRs (SHR-Cs) and normotensive Wistar rats were used as controls. Exercise training enhanced myocardial hypertrophy assessed by left ventricular weight/tibial length (228Ϯ7 versus 251Ϯ5 mg/cm in SHR-Cs and exercised SHRs [SHR-Es], respectively). Myocyte cross-sectional area increased Ϸ40%, collagen volume fraction decreased Ϸ50%, and capillary density increased Ϸ45% in SHR-Es compared with SHR-Cs. The mRNA abundance of atrial natriuretic factor and myosin light chain 2 was decreased by the swimming routine (100Ϯ19% versus 41Ϯ10% and 100Ϯ8% versus 61Ϯ9% for atrial natriuretic factor and myosin light chain 2 in SHR-Cs and SHR-Es, respectively). The expression of sarcoplasmic reticulum Ca 2ϩ pump was significantly augmented, whereas that of Na ϩ /Ca 2ϩ exchanger was unchanged (93Ϯ7% versus 167Ϯ8% and 158Ϯ13% versus 157Ϯ7%, sarcoplasmic reticulum Ca 2ϩ pump and Na ϩ /Ca 2ϩ exchanger in SHR-Cs and SHR-Es, respectively; PϽ0.05). Endurance training inhibited apoptosis, as reflected by a decrease in caspase 3 activation and poly(ADP-ribose) polymerase-1 cleavage, and normalized calcineurin activity without inducing significant changes in the phosphatidylinositol 3-kinase/Akt pathway. The swimming routine improved midventricular shortening determined by echocardiography (32.4Ϯ0.9% versus 36.9Ϯ1.1% in SHR-Cs and SHR-Es, respectively; PϽ0.05) and decreased the left ventricular free wall thickness/left ventricular cavity radius toward an eccentric model of cardiac hypertrophy (0.59Ϯ0.02 versus 0.53Ϯ0.01 in SHR-Cs and SHR-Es, respectively; PϽ0.05). In conclusion, we present data demonstrating the effectiveness of endurance training to convert pathological into physiological hypertrophy improving cardiac performance. The reduction of myocardial fibrosis and calcineurin activity plus the increase in capillary density represent factors to be considered in determining this beneficial effect.

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Section: Discussionmentioning

confidence: 55%

Endurance Training in the Spontaneously Hypertensive Rat

et al. 2009

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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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“…[1][2][3] The biological role of NPs in mild HF is underscored by reports that NP receptor antagonism in experimental mild HF results in RAAS activation and sodium retention, consistent with a role for NPs in mild HF to maintain sodium balance and suppress the RAAS. 4 Such a role is further supported by Lopez et al, 5 who demonstrated that genetic deletion of the receptor for ANP and BNP results in an impaired renal response to volume loading.…”

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confidence: 97%

Endogenous Natriuretic Peptides Participate in Renal and Humoral Actions of Acute Vasopeptidase Inhibition in Experimental Mild Heart Failure

et al. 2001

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Abstract-Mild heart failure is characterized by increases in atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in the absence of activation of the renin-angiotensin-aldosterone system (RAAS). Vasopeptidase (VP) inhibitors are novel molecules that coinhibit neutral endopeptidase 24.11, which degrades the natriuretic peptides (NPs) and ACE. In a well-characterized canine model of mild heart failure produced by ventricular pacing at 180 bpm for 10 days, we defined the renal and humoral actions of acute VP inhibition with omapatrilat (OMA, nϭ6) and acute ACE inhibition (nϭ5) alone with fosinoprilat. We also sought to determine whether the NPs participate in the renal actions of acute VP inhibition by the administration of OMA together with an intrarenal administration of the NP receptor antagonist HS-142-1 (nϭ5). OMA resulted in a greater natriuretic response than did ACE inhibition in association with increases in plasma cGMP, ANP, BNP, urinary cGMP, urinary ANP excretion, and glomerular filtration rate (PϽ0.05 for OMA versus ACE inhibition). Plasma renin activity was increased only in the group subjected to ACE inhibition. Administration of intrarenal HS-142-1 attenuated the renal properties of OMA in association with a decrease in urinary cGMP excretion despite similar increases in plasma ANP and BNP. This study provides new insight into a unique new pharmacological agent that has beneficial renal actions in experimental mild heart failure beyond the actions that are observed with ACE inhibition alone and that are linked to the NP system. Key Words: natriuretic peptides Ⅲ heart failure Ⅲ renin Ⅲ angiotensin M ild heart failure (HF) is the initial chronic compensated phase of left ventricular dysfunction, which is characterized by sodium balance and increases in the cardiac natriuretic peptides (NPs), atrial NP (ANP), and brain NP (BNP), without activation of the renin-angiotensin-aldosterone system (RAAS). 1-3 The biological role of NPs in mild HF is underscored by reports that NP receptor antagonism in experimental mild HF results in RAAS activation and sodium retention, consistent with a role for NPs in mild HF to maintain sodium balance and suppress the RAAS. 4 Such a role is further supported by Lopez et al, 5 who demonstrated that genetic deletion of the receptor for ANP and BNP results in an impaired renal response to volume loading.The only recommended therapy for mild HF is the use of ACE inhibition (ACEI), which is based on the Studies of Left Ventricular Dysfunction (SOLVD) trial and the Survival and Ventricular Enlargement (SAVE) study. 6,7 A major conclusion of the SOLVD trial was the need to identify new therapeutic strategies in mild HF based in part on the suboptimal impact of ACEI on mortality. 7 The SOLVD trial stated that "while ACEI was well tolerated by patients with asymptomatic left ventricular dysfunction (ALVD) and reduced the incidence of HF and related hospitalizations, the lack of a significant effect on overall mortality emphasizes the need to explore more effective ...

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Atrial natriuretic peptide in heart failure

Cited by 82 publications

References 38 publications

Endurance Training in the Spontaneously Hypertensive Rat

Endurance Training in the Spontaneously Hypertensive Rat

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

Endogenous Natriuretic Peptides Participate in Renal and Humoral Actions of Acute Vasopeptidase Inhibition in Experimental Mild Heart Failure

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