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European Journal of Heart Failure 2008 10(4):360-366; doi:10.1016/j.ejheart.2008.02.005
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© 2008 European Society of Cardiology

Effect of atrial natriuretic peptide on adiponectin in patients with heart failure

Toshinari Tanaka, Takayoshi Tsutamoto*, Hiroshi Sakai, Keizo Nishiyama, Masanori Fujii, Takashi Yamamoto and Minoru Horie

Cardiovascular and Respiratory Medicine, Shiga University of Medical Science Tsukinowa, Seta, Otsu 520-2192, Japan

* Corresponding author. Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Tsukinowa, Seta, Otsu 520-2192, Japan. Tel.: +81 77 548 2213; fax: +81 77 543 5839. E-mail address: tutamoto{at}belle.shiga-med.ac.jp (T. Tsutamoto).


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Background: The adipocyte-specific cytokine adiponectin, has cardioprotective effects, correlates with endogenous cardiac natriuretic peptides and adipocyte has guanylyl cyclase-A receptors of natriuretic peptides.

Aims: To evaluate the effect of carperitide (atrial natriuretic peptide; ANP) on plasma adiponectin in patients with heart failure.

Methods and results: Seventy-five patients admitted to our hospital with decompensated heart failure were randomised (1:2) to nitroglycerin (group I: n = 23) or carperitide infusion (group II: n = 52). Blood samples were collected at baseline and after 7 days. Plasma levels of total and high-molecular weight (HMW) adiponectin, ANP and brain natriuretic peptide (BNP) were measured. There were no differences in baseline characteristics between the two groups. In group I, plasma levels of total and HMW adiponectin were significantly decreased (21.1±2.5 to 18.6±2.5 µg/mL, p < 0.05, 12.3±1.8 to 10.8±1.7 µg/mL, p < 0.05, respectively) concomitant with the decrease in plasma levels of ANP and BNP. In group II, plasma levels of total and HMW adiponectin were significantly increased (17.3±1.3 to 19.7±1.6 µg/mL, p < 0.0001, 9.8±1.0 to 10.5±1.0 µg/mL, p < 0.05, respectively) concomitant with the increase in ANP.

Conclusions: These findings indicate that carperitide infusion increases plasma levels of total and HMW adiponectin in patients with heart failure.

Key Words: Adiponectin • Carperitide • Atrial natriuretic peptide • Brain natriuretic peptide • Heart failure

Received August 15, 2007; Revised November 9, 2007; Accepted February 4, 2008


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
Adiponectin, which is an adipocyte-specific cytokine, inhibits the inflammatory process and atherosclerotic actions [1], and plays a central role in both glucose and lipid metabolism [2,3]. In addition, adiponectin inhibits hypertrophic signalling in the myocardium through activation of AMP-activated protein kinase signalling, and has a beneficial effect in cardiovascular diseases [4]. Shibata et al. reported that adiponectin-deficient mice showed an increased infarct size, whereas exogenous adiponectin reduced infarct size in both adiponectin-deficient mice and wild-type mice, suggesting that adiponectin protects the heart post myocardial infarction [5]. Moreover, pressure overload in adiponectin-deficient mice resulted in enhanced cardiac hypertrophy and increased mortality, whereas exogenous adiponectin attenuated cardiac hypertrophy in response to pressure overload in adiponectin-deficient mice [4].

As adiponectin is markedly downregulated in obesity-linked diseases [6] such as coronary artery disease [7,8] and type 2 diabetes [9], and inversely correlated with body mass index (BMI) [9], promoting the risk for developing heart failure [10], procedures to increase adiponectin could potentially be beneficial in patients with chronic heart failure (CHF) due to coronary artery disease [5] and hypertensive heart disease [4]. Clinical studies including our recent study have suggested a positive correlation between the plasma levels of cardiac natriuretic peptides, such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), and adiponectin in patients with coronary artery disease [11] and in patients with CHF [12,13]. Studies have also suggested that cardiac natriuretic peptides have a novel lipolytic and potential lipid-mobilization effect that is mediated by a guanylyl cyclase-A (GC-A) receptor[14-16]. In addition, a recent preliminary study [17] showed that BNP increases adiponectin mRNA in cultured adipocytes via a functional GC-A receptor.

Adiponectin circulates in plasma as a trimer, a hexamer, and in a high-molecular weight (HMW) form [18,19]. Recent studies have suggested that HMW adiponectin is an active form of this protein and that HMW adiponectin is superior to total adiponectin as a predictor of metabolic abnormalities [20,21]. However, whether exogenous cardiac natriuretic peptides are useful for the treatment of decompensated heart failure [22-26] and acute myocardial infarction [27], and whether they can increase the plasma levels of total and HMW adiponectin, remains unknown.

The present study evaluated whether synthetic ANP (carperitide) infusion can increase the plasma levels of total and HMW adiponectin in patients with heart failure.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
2.1. Patients
Patients admitted to our institution with decompensated heart failure [left ventricular ejection fraction (LVEF) measured by two-dimensional echocardiography <45%] and New York Heart Association (NYHA) functional class III or IV, were eligible to be included in this study. Patients with severe heart failure who needed cardiac resynchronization therapy, an implantable cardioverter-defibrillator or other mechanical support were excluded. Patients with unstable angina pectoris, renal failure (serum creatinine>2.0 mg/dL) or liver dysfunction were also excluded. Patients with cardiogenic shock or hypotension defined as systolic blood pressure <90 mm Hg were excluded. Moreover, patients who were receiving pioglitazone hydrochloride or telmisartan, which are ligands of the peroxisome proliferator-activated receptor {gamma}, were also excluded.

Seventy-five HF patients were included in the study and were randomised (1:2) to nitroglycerin (NTG) or carperitide infusion.

2.2. Study protocol
On admission, blood sampling for measurement of plasma levels of total adiponectin and HMW adiponectin and plasma levels of ANP and BNP was performed. Most patients were already receiving standard oral therapy for heart failure. In patients treated with NTG (group I), infusion of NTG was started at a dose of 0.2 {varepsilon}g/kg/min. If the systolic blood pressure was high (>150 mm Hg) or low (<90 mm Hg), doses of NTG were adjusted to maintain constant blood pressure (mean 0.24±0.04 {varepsilon}g/kg/min) as previously reported [27]. In patients receiving carperitide (group II), the carperitide infusion was started at a dose of 0.02 {varepsilon}g/kg/min, the dose was then adjusted to 0.01-0.1 {varepsilon}g/kg/min within 24 h (mean 0.019±0.002 {varepsilon}g/kg/min) to maintain a systolic blood pressure above 90 mm Hg, as previously reported [26]. Infusions of the two drugs were continued for 7 days. In both groups, physicians could administer intravenous loop diuretics and catecholamines as deemed appropriate. Plasma levels of total adiponectin and HMW adiponectin and plasma levels of ANP and BNP were measured after 7 days in both groups. Plasma total adiponectin level was measured by a sandwich ELISA system (adiponectin ELISA kit, Otsuka Pharmaceutical Co Ltd) [6,13]. Plasma HMW adiponectin concentration was measured using a sandwich ELISA based on a monoclonal antibody to human HMW adiponectin (Fujirebio ELISA kit, Tokyo, Japan) [13,20]. Plasma concentrations of ANP and BNP were measured with a specific immunoradiometric assay for human ANP and BNP using a commercial kit (Shionogi, Osaka, Japan) as previously reported [28]. Renal function was represented by the estimated glomerular filtration rate (eGFR) according to the Cockcroft-Gault equation. Informed consent was obtained from all patients for participation in the study, according to a protocol approved by the Committee on Human Investigation at our institution.

2.3. Statistical analysis
All results are expressed as the mean±SEM. A chi-square test was used to determine differences between groups. Univariate analyses were performed between two groups using Student's t test. Because plasma levels of ANP and BNP were not normally distributed, differences in mean levels of ANP and BNP between the two groups were tested by Wilcoxon rank-sum test for paired values and by Mann-Whitney U test for unpaired values and log ANP and log BNP were used to determine correlations and regression models. Non-parametric spearman's correlation method was used for correlation analysis. A two- tailed probability value of <0.05 was considered significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
3.1. Clinical characteristics at baseline
Seventy-five severe heart failure patients were randomised to NTG (group I, n=23) or carperitide infusion (group II, n=52). There was no difference in age, gender, NYHA functional class, BMI, heart rate, mean blood pressure, eGFR, ANP, BNP, norepinephrine or total and HMW adiponectin between the two groups at baseline (Table 1). In group II, the average dose of carperitide was 0.019±0.002 {varepsilon}g/kg/min. Except for carperitide infusion, there were no differences in treatment between the two groups.


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  		Table 1 Comparison of baseline characteristics between patients treated with and without carperitide

 
At baseline, there were positive significant correlation between the plasma levels of total adiponectin and log ANP (rspearman=0.248, p<0.05) and log BNP (rspearman=0.261, p<0.05) in the whole patient population (group I+group II).

3.2. Total and HMW adiponectin before and after 7 days of treatment for heart failure
Seven days after commencing treatment for heart failure, there were no significant differences in NYHA functional class, BMI, body weight, heart rate, blood pressure, serum creatinine, eGFR or BNP between the two groups (Table 2). In group I, plasma levels of total and HMW adiponectin were significantly decreased (21.1±2.5 to 18.6±2.5 {varepsilon}g/mL, p<0.05, 12.3±1.8 to 10.8±1.7 {varepsilon}g/mL, p<0.05, respectively) (Fig. 1) concomitant with a significant decrease in the plasma levels of ANP and BNP (289±48 to 144±34 pg/mL, p<0.001, 969±231 to 692±253 pg/mL, p<0.001, respectively) (Fig. 2). In group II, plasma levels of total and HMW adiponectin were significantly increased (17.3±1.3 to 19.7±1.6 {varepsilon}g/mL, p<0.0001, 9.8±1.0 to 10.5±1.0 {varepsilon}g/mL, p<0.05, respectively) (Fig. 1) concomitant with the significant increase in ANP (249±33 to 542±78 pg/mL, p<0.0001) and decrease in BNP (863±98 to 460±62 pg/mL, p<0.0001) (Fig. 2). Seven days after treatment, percent change in total adiponectin was significantly higher in group II than in group I (+14.5±3.0% vs. –13.2±5.2%, p<0.0001) and delta percent change in HMW adiponectin was also significantly higher in group II than in group I (+10.0±3.4% vs. –10.8±6.1%, p=0.0116) (Fig. 3). There was significant positive correlation between the change in ANP levels and the change in plasma adiponectin levels in all groups (r=0.258, p<0.05).


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  		Table 2 Changes in BMI, NYHA functional class, renal function, total and HMW adiponectin from baseline to 7 days treatment for heart failure

 


Figure 01
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  		Fig. 1 Comparisons of plasma levels of total and high-molecular weight (HMW) adiponectin at baseline and after 7 days of treatment for heart failure. Group I=nitroglycerin infusion (n=23). Group II=carperitide infusion (n=52). {dagger}: p<0.05, *: p<0.0001 vs. the baseline value.

 


Figure 02
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  		Fig. 2 Comparisons of plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) at baseline and after 7 days of treatment for heart failure. Group I=nitroglycerin infusion (n=23). Group II=carperitide infusion (n=52). The black boxes indicate the value of plasma ANP and the white boxes indicate plasma BNP. Each box defines the interquartile range with the median indicated by the crossbar. *: p<0.001, {dagger}: p<0.0001 vs. the baseline value.

 


Figure 03
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  		Fig. 3 Comparisons of the percent delta change in total and high-molecular weight (HMW) adiponectin in patients receiving 7-days treatment for heart failure. Group I=nitroglycerin infusion (n=23). Group II=carperitide infusion (n=52). Percent delta change=[(after-baseline)/baseline]x100 (%).

 
3.3. Comparisons of the change in body mass index and change in plasma adiponectin levels after 7 days of treatment
At baseline, there was a significant correlation between BMI and total adiponectin in all patients (r=–0.388, p<0.01, Fig. 4). Seven days after treatment, there was no difference in delta change of BMI between the two groups (group I; –5.3±0.7%, group II; –4.3±0.4%, p=0.165), and delta changes in total adiponectin and HMW adiponectin were significantly higher in group II than in group I (Fig. 3). In group I, there was no correlation between the change in BMI and the change in plasma adiponectin level after 7 days of treatment for heart failure (r=–0.113, p=0.616). In contrast, in group II, there was a significant correlation between the change in BMI and the change in plasma adiponectin level (r=–0.402, p<0.001) (Fig. 4).


Figure 04
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  		Fig. 4 Correlation between total adiponectin and body mass index (BMI) at baseline in the overall patient population (group I+group II) and comparisons between the change in adiponectin and the change in BMI in each group. Open circles represent the patients in group I (nitroglycerin infusion, n=23) and closed circles represent the patients in group II (carperitide infusion, n=52). Delta change in total adiponectin=(after-baseline) total adiponectin level and delta change in BMI=(after-baseline) BMI.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
Our study demonstrates for the first time that exogenous ANP (carperitide) infusion for 7 days increased plasma total and HMW adiponectin. There was also a significant positive correlation between the change in ANP levels and the change in plasma adiponectin levels in all groups before and after treatment for heart failure. In addition, plasma levels of adiponectin were significantly decreased after the infusion of ANP was discontinued (data not shown). In contrast, plasma total and HMW adiponectin levels decreased after NTG infusion in association with a decrease in endogenous natriuretic peptide (ANP, BNP), suggesting a significant relationship between cardiac natriuretic peptides and adiponectin in heart failure. Our findings may be supported by studies showing that cardiac natriuretic peptides have a novel lipolytic and potential lipid-mobilizing effect that is mediated by a GC-A receptor [14-16] and that BNP increases adiponectin mRNA in cultured adipocytes via GC-A [17].

Recently, we performed a study to evaluate whether haemodynamic abnormalities contributed directly to elevated total adiponectin. In the study, 449 CHF patients were evaluated using a Swan-Ganz catheter; results showed that there were no haemodynamic parameters that were independently associated with an elevation in either total or HMW adiponectin [13]. On multivariable analyses, low BMI, high plasma BNP level, female gender, and absence of diabetes mellitus were significant independent predictors of high plasma total and HMW adiponectin [13]. Taken together with our recent findings, this suggests that changes in total and HMW adiponectin after 7 days of treatment with carperitide were mainly due to changes in cardiac natriuretic peptides.

Previous studies have reported that plasma adiponectin levels are high in patients with chronic renal failure compared to healthy controls [29,30], suggesting that changes in renal function may also have influenced the plasma adiponectin levels in this study. Since renal function deteriorated after treatment for heart failure [31,32] in both groups in our study, the contrasting changes in total and HMW adiponectin are unlikely to be due to differences in renal function.

Regarding the time course of changes in adiponectin levels; patients in previous studies that evaluated the effect of hypocaloric diet [33], exercise [34], or medication [35] on adiponectin levels over several months had normal cardiac function and no fluid retention. In the present study, most heart failure patients had some fluid retention; however, it is difficult to evaluate the level of excess fluid retention in individual patients, and body weight changes consisted of both fluid reduction and changes in metabolism including lipid-mobilization. In the present study, plasma adiponectin levels were changed after 7 days of treatment for heart failure, and were accompanied by a significant decrease in body weight. Although the half-life of plasma adiponectin remains unknown in patients with heart failure, our observations support the findings that the half-life of plasma adiponectin is several hours in animal models [36,37].

Significant negative correlations between BMI and adiponectin have been reported in the general population and in patients with heart failure. In the present study, there was a negative correlation between BMI and adiponectin at baseline (Fig. 4). Interestingly, there were significant correlations between changes in BMI and changes in plasma adiponectin levels in patients receiving ANP (carperitide) infusion, but not in those receiving NTG infusion (Fig. 4). The mechanisms underlying these findings remain unexplained at present. The body weight decrease associated with the decrease in adiponectin in patients on non-carperitide treatment may not be a physiological change, while the body weight decrease associated with the increased adiponectin in patients who received carperitide may be a physiological change.

We speculate that carperitide increases the production of adiponectin but could not evaluate the source of the increase in adiponectin. In addition, we could not estimate the acute effect of carperitide and the dose response of carperitide on plasma adiponectin. Therefore, further studies are needed to evaluate these findings. However, treatments which increase total and HMW adiponectin may have cardioprotective effects because adiponectin stimulates myocardial AMPK signalling, leading to suppression of myocyte hypertrophy and apoptosis and because adiponectin also stimulates COX-2 expression, resulting in a reduction of cardiac inflammation [5]. Increases in plasma adiponectin have been reported with angiotensin-converting enzyme inhibitors [38] and angiotensin receptor blockers [38,39]. These agents have shown a beneficial effect on mortality and morbidity in patients with CHF [40,41].

Adiponectin has a beneficial effect on metabolic abnormalities [42] and ventricular remodelling [4,43]; however, a high adiponectin level has been reported to be associated with high mortality in CHF patients [12,13]. Therefore, further studies are needed to evaluate the long-term cardiovascular effects of treatments to increase plasma adiponectin, including carperitide administration. Several clinical studies have demonstrated that the administration of exogenous ANP or BNP is useful for the treatment of CHF [22-26] or acute myocardial infarction [27] and that these beneficial effects of ANP and BNP may be partly due to the effect on total and HMW adiponectin.

An increase in adiponectin is a favourable finding in cardiac disease patients; however, previous studies have also demonstrated the role of total adiponectin level as a marker of mortality in heart failure [12,13]. It is not easy to explain this paradox. An important message from this study may be the limitation of using total adiponectin level for assessing prognosis in heart failure. Since an increase in total adiponectin level, but a decrease in BNP and an improvement in NYHA functional class were observed in our patients treated with ANP (carperitide), total adiponectin level may not predict the prognosis of heart failure in such patients. Further study is needed to clarify this issue.

In conclusion, non-carperitide treatment decreases the plasma levels of total and HMW adiponectin and synthetic ANP (carperitide) infusion can increase the plasma levels of total and HMW adiponectin in patients with heart failure.


   Acknowledgements
 
We wish to thank Ms. Aoi Murata for her excellent technical assistance. We also express thanks to Mr. Daniel Mrozek for assistance in preparing the manuscript. This study was supported by a Grant-in-Aid for Scientific Research in Japan.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 

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