Wall stress modulates brain natriuretic peptide production in pressure overload cardiomyopathy

Vanderheyden, Marc; Goethals, Marc; Verstreken, Sofie; Bruyne, Bernard De; Müller, Kristin; Schuerbeeck, Eddy Van; Bartúnek, Jozef

doi:10.1016/j.jacc.2004.09.038

Cited by 165 publications

(142 citation statements)

References 40 publications

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“…For example, BNP expression undergoes compensatory upregulation under stressed conditions of the heart, including heart failure and cardiac hypertrophy. 25,26 BNP transgenic mice exhibit attenuated albuminuria and renal damage after subtotal nephrectomy, 27 and the overexpression of BNP in mice also improves immune-mediated renal injury. 28 Adrenomedullin is abundantly expressed in heart tissue and upregulated by cardiac stress, including pressure overload and myocardial infarction.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Myocyte-Derived Follistatin-Like 1 Prevents Renal Injury in a Subtotal Nephrectomy Model

Hayakawa¹,

Ohashi

Shibata³

et al. 2015

Journal of the American Society of Nephrology

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Heart disease contributes to the progression of CKD. Heart tissue produces a number of secreted proteins, also known as cardiokines, which participate in intercellular and intertissue communication. We recently reported that follistatin-like 1 (Fstl1) functions as a cardiokine with cardioprotective properties. Here, we investigated the role of cardiac Fstl1 in renal injury after subtotal nephrectomy. Cardiac-specific Fstl1-deficient (cFstl1-KO) mice and wild-type mice were subjected to subtotal (5/6) nephrectomy. cFstl1-KO mice showed exacerbation of urinary albumin excretion, glomerular hypertrophy, and tubulointerstitial fibrosis after subtotal renal ablation compared with wild-type mice. cFstl1-KO mice also exhibited increased mRNA levels of proinflammatory cytokines, including TNF-a and IL-6, NADPH oxidase components, and fibrotic mediators, in the remnant kidney. Conversely, systemic administration of adenoviral vectors expressing Fstl1 (Ad-Fstl1) to wild-type mice with subtotal nephrectomy led to amelioration of albuminuria, glomerular hypertrophy, and tubulointerstitial fibrosis, accompanied by reduced expression of proinflammatory mediators, NADPH oxidase components, and fibrotic markers in the remnant kidney. In cultured human mesangial cells, treatment with recombinant FSTL1 attenuated TNF-a-stimulated expression of proinflammatory cytokines. Treatment of mesangial cells with FSTL1 augmented the phosphorylation of AMP-activated protein kinase (AMPK), and inhibition of AMPK activation abrogated the anti-inflammatory effects of FSTL1. These data suggest that Fstl1 functions in cardiorenal communication and that the lack of Fstl1 production by myocytes promotes glomerular and tubulointerstitial damage in the kidney.

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Section: Discussionmentioning

confidence: 99%

Cardiac Myocyte-Derived Follistatin-Like 1 Prevents Renal Injury in a Subtotal Nephrectomy Model

Hayakawa¹,

Ohashi

Shibata³

et al. 2015

Journal of the American Society of Nephrology

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“…2,3,16 It has been suggested that LV end-diastolic wall stress is the most important hemodynamic parameter regulating the levels of circulating BNP. 12,17 Of note, circulating BNP reflects the balance between BNP release and elimination. In contrast, our data suggest that LVESWS is the key loading parameter for ⌬ A-CS BNP, that is, cardiac BNP release, indicating that LV geometry and afterload rather than filling pressures are the most important mechanical determinants of cardiac BNP release.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, our data suggest that LVESWS is the key loading parameter for ⌬ A-CS BNP, that is, cardiac BNP release, indicating that LV geometry and afterload rather than filling pressures are the most important mechanical determinants of cardiac BNP release. The strength of our study compared with previous ones evaluating the relationship between plasma BNP levels and wall stress 12,17 lies in the fact that we studied subjects with a broad range of LV dysfunction, including a group with normal LVEF and normal LV diastolic function. Most importantly, in our study we measured ⌬ A-CS BNP rather than peripheral BNP.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic Determinants of Myocardial B-Type Natriuretic Peptide Release

2010

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Abstract-Although B-type natriuretic peptide (BNP) is widely used as a biomarker for heart failure, the in vivo mechanical stimulus for its cardiac release remains poorly defined. We aimed to characterize the hemodynamic determinants of the transcardiac BNP gradient as a measure of myocardial BNP release by performing a detailed hemodynamic assessment in subjects with a broad spectrum of systolic and diastolic left ventricular dysfunction. Forty-two subjects underwent a detailed transthoracic echocardiographic study, right heart catheterization, and simultaneous BNP measurement in arterial and coronary sinus plasma. The transcardiac BNP gradient was lowest in subjects with normal left ventricular ejection fraction/high peak early diastolic annular velocity (nϭ11), intermediate in those with normal left ventricular ejection fraction/low peak early diastolic annular velocity (nϭ13), and highest in those with low left ventricular ejection fraction/low peak early diastolic annular velocity (nϭ18; 29 ng/L (range: 15 to 78 ng/L) versus 88 ng/L (range: 34 to 172 ng/L) versus 1566 ng/L (range: 624 to 2349 ng/L; PϽ0.001). Across the range of patients, left ventricular end-systolic wall stress (r 2 ϭ0.51) and peak systolic mitral annular velocity (r 2 ϭ0.47) showed the strongest correlation with higher transcardiac BNP gradient. In contrast, the transcardiac BNP gradient was weakly related to indices of diastolic load, including pulmonary capillary wedge pressure (r 2 ϭ0.27) and left ventricular end-diastolic wall stress (r 2 ϭ0.21). Across this spectrum of pathophysiology, left ventricular end-systolic wall stress appears to be the key mechanical stimulus influencing cardiac BNP release. (Hypertension. 2010;56:682-689.)

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“…However, at a later stage, when this compensatory mechanism is overridden, LV wall stress and filling pressure increase triggering BNP activation and release. 19 In symptomatic AS, BNP release has been shown to reflect the elevation in LV filling pressures. 20 In symptomatic or asymptomatic severe AS with structural impairment such as diastolic dysfunction, LA dilatation, LV hypertrophy, and fibrosis, elevated single BNP level measurement is a marker of already elevated LV filling pressures predicting poor short-term outcome.…”

Section: Pathophysiology Of Bnp Release In Asmentioning

confidence: 99%

Impact of Serial B-Type Natriuretic Peptide Changes for Predicting Outcome in Asymptomatic Patients With Aortic Stenosis

Henri

Magné

Caballero

et al. 2016

Canadian Journal of Cardiology

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Background: The aim of this study was to determine the impact on the outcome of serial B-type natriuretic peptide (BNP) changes during follow-up in asymptomatic patients with ! moderate aortic stenosis (AS) and preserved left ventricular ejection fraction. Methods: We prospectively screened 69 patients who underwent comprehensive transthoracic echocardiography, BNP level measurement at baseline and after every 6 or 12 months. Annualized BNP changes were calculated as the difference between the last and baseline BNP measurements divided by the duration of follow-up. The primary endpoint was the occurrence of symptoms, aortic valve replacement, or cardiovascular death. Results: During a follow-up of 30 AE 19 months, 43 patients experienced a cardiac event. These patients were significantly older (73 AE 9

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Wall stress modulates brain natriuretic peptide production in pressure overload cardiomyopathy

Abstract: In patients with AS, BNP appears to be regulated not only by systolic but also by diastolic load. This supports the hypothesis that myocardial stretch modulates BNP production in human pressure overload hypertrophy/failure.

Cited by 165 publications

References 40 publications

Cardiac Myocyte-Derived Follistatin-Like 1 Prevents Renal Injury in a Subtotal Nephrectomy Model

Cardiac Myocyte-Derived Follistatin-Like 1 Prevents Renal Injury in a Subtotal Nephrectomy Model

Hemodynamic Determinants of Myocardial B-Type Natriuretic Peptide Release

Impact of Serial B-Type Natriuretic Peptide Changes for Predicting Outcome in Asymptomatic Patients With Aortic Stenosis

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