BNP gene expression is specifically modulated by stretch and ET-1 in a new model of isolated rat atria

Bruneau, Benoit G.; Piazza, Leonardo A.; Bold, Adolfo J. de

doi:10.1152/ajpheart.1997.273.6.h2678

Cited by 69 publications

(64 citation statements)

References 23 publications

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“…1C). BNP is produced by and released from ventricular cardiomyocytes (Bruneau et al, 1997), and plasma levels of BNP are closely linked to the severity of ventricular remodeling and dysfunction (Sztrymf et al, 2010;McLaughlin et al, 2013). The effect of RAN in reducing BNP in our study is consistent with the benefits of RAN in animal models of left-sided heart disease as well as with the amelioration of RV failure in this animal model (Aistrup et al, 2013;Guihaire et al, 2013;McLaughlin et al, 2013).…”

Section: Ranolazine Reduces Cardiac Remodeling In Pah Ratssupporting

confidence: 86%

Ranolazine Reduces Remodeling of the Right Ventricle and Provoked Arrhythmias in Rats with Pulmonary Hypertension

Liles

Hoyer

Oliver

et al. 2015

J Pharmacol Exp Ther

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Pulmonary arterial hypertension (PAH) is a progressive disease that often results in right ventricular (RV) failure and death. During disease progression, structural and electrical remodeling of the right ventricle impairs pump function, creates proarrhythmic substrates, and triggers for arrhythmias. Notably, RV failure and lethal arrhythmias are major contributors to cardiac death in patients with PAH that are not directly addressed by currently available therapies. Ranolazine (RAN) is an antianginal, antiischemic drug that has cardioprotective effects in experimental and clinical settings of left-sided heart dysfunction. RAN also has antiarrhythmic effects due to inhibition of the late sodium current in cardiomyocytes. We therefore hypothesized that RAN could reduce the maladaptive structural and electrical remodeling of the right ventricle and could prevent triggered ventricular arrhythmias in the monocrotaline rat model of PAH. Indeed, in both in vivo and ex vivo experimental settings, chronic RAN treatment reduced electrical heterogeneity (right ventricular-left ventricular action potential duration dispersion), shortened heart-rate corrected QT intervals in the right ventricle, and normalized RV dysfunction. Chronic RAN treatment also dose-dependently reduced ventricular hypertrophy, reduced circulating levels of B-type natriuretic peptide, and decreased the expression of fibrotic markers. In addition, the acute administration of RAN prevented isoproterenol-induced ventricular tachycardia/ventricular fibrillation and subsequent cardiovascular death in rats with established PAH. These results support the notion that RAN can improve the electrical and functional properties of the right ventricle, highlighting its potential benefits in the setting of RV impairment.

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Section: Ranolazine Reduces Cardiac Remodeling In Pah Ratssupporting

confidence: 86%

Ranolazine Reduces Remodeling of the Right Ventricle and Provoked Arrhythmias in Rats with Pulmonary Hypertension

Liles

Hoyer

Oliver

et al. 2015

J Pharmacol Exp Ther

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“…[25][26][27] Several neuroendocrine mechanisms also mediate cardiac BNP release. 28,29 For example, α-adrenergic stimulation with phenylephrine results in increases in both BNP gene expression and BNP secretion, whereas myocardial stretch and endothelin-1 (ET-1) induce a marked increase in BNP gene expression alone. 29,30 Atrial myocytes store pre-synthesized ANP and BNP in secretory granules and release them via a regulated pathway.…”

Section: Dovepressmentioning

confidence: 99%

Brain natriuretic peptide in pulmonary arterial hypertension: biomarker and potential therapeutic agent

Casserly

Klinger²

2009

DDDT

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B-type natriuretic peptide (BNP) is a member of the natriuretic peptide family, a group of widely distributed, but evolutionarily conserved, polypeptide mediators that exert myriad cardiovascular effects. BNP is a potent vasodilator with mitogenic, hypertrophic and pro-inflammatory properties that is upregulated in pulmonary hypertensive diseases. Circulating levels of BNP correlate with mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR) in patients with pulmonary arterial hypertension (PAH). Elevated plasma BNP levels are associated with increased mortality in patients with PAH and a fall in BNP levels after therapy is associated with improved survival. These findings have important clinical implications in that a noninvasive blood test may be used to identify PAH patients at high-risk of decompensation and to guide pulmonary vasodilator therapy. BNP also has several biologic effects that could be beneficial to patients with PAH. However, lack of a convenient method for achieving sustained increases in circulating BNP levels has impeded the development of BNP as a therapy for treating pulmonary hypertension. New technologies that allow transdermal or oral administration of the natriuretic peptides have the potential to greatly accelerate research into therapeutic use of BNP for cor pulmonale and pulmonary vascular diseases. This review will examine the basic science and clinical research that has led to our understanding of the role of BNP in cardiovascular physiology, its use as a biomarker of right ventricular function and its therapeutic potential for managing patients with pulmonary vascular disease.

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“…[1][2][3] Among them, several mediators, such as TNF-a, IL-1 and endothelin-1, can induce the production and secretion of BNP. [28][29][30] Thus, there is a possibility that BNP is involved in the pathogenesis of VOD. In addition, accumulating evidence suggests that transient LV systolic dysfunction in the absence of coronary artery disease can occur in patients with acute medical illness, especially those treated in intensive care units.…”

Section: Discussionmentioning

confidence: 99%

Plasma brain natriuretic peptide is associated with hepatic veno-occlusive disease and early mortality after allogeneic hematopoietic stem cell transplantation

Kataoka

Nannya

Iwata

et al. 2010

Bone Marrow Transplant

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Fluid retention is characteristic of veno-occlusive disease (VOD). We hypothesized that plasma brain natriuretic peptide (BNP), a neurohormone secreted in response to volume expansion, may be associated with VOD after hematopoietic stem cell transplantation (HSCT). BNP was measured before and weekly after HSCT in 46 recipients. Sixteen patients developed VOD. BNP concentrations were similar before and on day 0 in patients with and without VOD, but were significantly higher on day 7 and later in those with VOD. Patients with VOD had significantly higher peak BNP concentrations before engraftment than those without VOD (median, 634.4 versus 80.9 pg ml À1; P ¼ 0.01). Multivariate analysis showed that VOD was independently associated with BNP elevation (odds ratio, 50.1; 95% CI: 5.2-478.4; Po0.01). Landmark analysis at day 7 showed that patients with peak BNP concentration of X180 pg ml À1 had significantly worse 100-day survival than patients with peak BNP o180 pg ml À1 (54 versus 91%; Po0.01). In multivariate analysis, BNP elevation before day 7 significantly predicted 100-day survival (hazard ratio 5.3; 95% CI: 1.1-24.3; P ¼ 0.03). These findings suggest that plasma BNP may serve as a diagnostic and prognostic marker of VOD.

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BNP gene expression is specifically modulated by stretch and ET-1 in a new model of isolated rat atria

Cited by 69 publications

References 23 publications

Ranolazine Reduces Remodeling of the Right Ventricle and Provoked Arrhythmias in Rats with Pulmonary Hypertension

Ranolazine Reduces Remodeling of the Right Ventricle and Provoked Arrhythmias in Rats with Pulmonary Hypertension

Brain natriuretic peptide in pulmonary arterial hypertension: biomarker and potential therapeutic agent

Plasma brain natriuretic peptide is associated with hepatic veno-occlusive disease and early mortality after allogeneic hematopoietic stem cell transplantation

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