Recombinant B-type Natriuretic Peptide Nesiritide Attenuates Vascular Remodelling by Reducing Plasma Aldosterone in Rabbits

Li, Shuqin; Xie, Hua; Yan, Huang-Ying; Lu, Yi; Wang, Lexin

doi:10.1016/j.hlc.2012.04.013

Cited by 9 publications

(12 citation statements)

References 20 publications

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“…BNP is a member of the natriuretic peptide family, a group of polypeptide mediators that exert pleiotropic cardiovascular effects. In addition to its vasodilative effects, an expanding body of literature suggests its role in the prevention of cardiovascular remodeling, such as its anti‐remodeling effects on systemic vasculatures and anti‐hypertrophic effects on myocardium . However, whether it has similar effect in pulmonary vascular system and through what mechanisms these effects are mediated remain to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, a recent study demonstrates that BNP can attenuate vascular remodeling induced by balloon injury rabbit iliac arteries. 12 In addition, we have recently demonstrated that high BNP levels are associated with the patency of ductus arteriosus and poor response to indomethacin, implicating its role in the inhibition of ductus arteriosus closure or remodeling in neonates. 13 However, little is known regarding its anti-remodeling effects on pulmonary vascular system.…”

Section: Introductionmentioning

confidence: 97%

“…In addition to its vasorelaxant effects, emerging evidence demonstrates that BNP has anti‐proliferative effects on human aortic vascular smooth muscle cells, suggesting its potential role in inhibiting vascular remodeling. Indeed, a recent study demonstrates that BNP can attenuate vascular remodeling induced by balloon injury rabbit iliac arteries . In addition, we have recently demonstrated that high BNP levels are associated with the patency of ductus arteriosus and poor response to indomethacin, implicating its role in the inhibition of ductus arteriosus closure or remodeling in neonates .…”

Section: Introductionmentioning

confidence: 99%

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B-type natriuretic peptide inhibits angiotensin II-induced proliferation and migration of pulmonary arterial smooth muscle cells

et al. 2013

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Pulmonary vascular remodeling, characterized by disordered proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs), is a pathognomonic feature of pulmonary arterial hypertension. Thus, pharmacologic strategy targeting on anti-proliferation and anti-migration of PASMCs may have therapeutic implications for PAH. Here we investigated the effects and underlying mechanisms of B-type natriuretic peptide (BNP) on angiotensin II (Ang II)-induced proliferation and migration of PASMCs. Proliferation and migration of PASMCs cultured from Wistar rats were induced by Ang II, with or without BNP treatment. In addition, potential underlying mechanisms including cell cycle progression, Ca(2+) overload, reactive oxygen species (ROS) production, signal transduction of MAPK and Akt, and the cGMP/PKG pathway were examined. We found that BNP inhibited Ang II-induced PASMCs proliferation and migration dose dependently. BNP could also arrest the cell cycle progression in the G0/G1-phase. In addition, BNP attenuated intracellular calcium overload caused by Ang II. Moreover, Ang II-induced ROS production was mitigated by BNP, with associated down-regulation of NAD(P)H oxidase 1 (Nox1) and reduced mitochondrial ROS production. Finally, Ang II-activated MAPKs and Akt were also counteracted by BNP. Of note, all these effects of BNP were abolished by a PKG inhibitor (Rp-8-Br-PET-cGMPS). In conclusion, BNP inhibits Ang II-induced PASMCs proliferation and migration. These effects are potentially mediated by decreased calcium influx, reduced ROS production by Nox1 and mitochondria, and down-regulation of MAPK and Akt signal transduction, through the cGMP/PKG pathway. Therefore, this study implicates that BNP may have a therapeutic role in pulmonary vascular remodeling.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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B-type natriuretic peptide inhibits angiotensin II-induced proliferation and migration of pulmonary arterial smooth muscle cells

et al. 2013

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“…Nesiritide inhibits vasoactive peptide production and displays high diuretic/natriuretic activity [51,52]. Importantly, nesiritide reduces cardiac toxicity by activating the neuroendocrine system [53]. Our present study showed that dobutamine is less effective than nesiritide, based on the data pooled from seven published studies.…”

Section: Studies Included In Quantitative Synthesis (Meta-analysis) (mentioning

confidence: 47%

Dobutamine Therapy is Associated with Worse Clinical Outcomes Compared with Nesiritide Therapy for Acute Decompensated Heart Failure: A Systematic Review and Meta-Analysis

Wang

Zhu

Shan³

2015

Am J Cardiovasc Drugs

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“…In addition to its vasorelaxant effects, emerging evidence demonstrates that BNP has anti-proliferative effects on human aortic vascular smooth muscle cells, suggesting its potential role in inhibiting vascular remodeling [ 32 36 ]. Indeed, a recent study demonstrates that BNP can attenuate vascular remodeling induced by balloon injury rabbit iliac arteries [ 37 ]. In addition, we have recently demonstrated that high BNP levels are associated with the patency of ductus arteriosus and poor response to indomethacin, implicating its role in the inhibition of ductus arteriosus closure or remodeling in neonates [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Reduced immunoreactivities of B-type natriuretic peptide in pulmonary arterial hypertension rats after ranolazine treatment

et al. 2016

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Pulmonary arterial hypertension (PAH) is a severe pulmonary vascular disease characterized by sustained increase in the pulmonary arterial pressure and excessive thickening and remodeling of the distal small pulmonary arteries. During disease progression, structural remodeling of the right ventricular (RV) impairs pump function, creates pro-arrhythmic substrates and triggers for arrhythmias. Notably, RV failure and lethal arrhythmias are major contributors to cardiac death in PAH that are not directly addressed by currently available therapies. Ranolazine (RAN) is an anti-anginal, anti-ischemic drug that has cardioprotective effects of heart dysfunction. RAN also has anti-arrhythmic effects due to inhibition of the late sodium current in cardiomyocytes. Therefore, we hypothesized that RAN could reduce the mal-adaptive structural remodeling of the RV, and prevent triggered ventricular arrhythmias in the monocrotaline-induced rat model of PAH. RAN reduced ventricular hypertrophy, reduced levels of B-type natriuretic peptide, and decreased the expression of fibrosis. In addition, RAN prevented cardiovascular death in rat model of PAH. These results support the notion that RAN can improve the functional properties of the RV, highlighting its potential benefits in the setting of heart impairment.

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Recombinant B-type Natriuretic Peptide Nesiritide Attenuates Vascular Remodelling by Reducing Plasma Aldosterone in Rabbits

Cited by 9 publications

References 20 publications

B-type natriuretic peptide inhibits angiotensin II-induced proliferation and migration of pulmonary arterial smooth muscle cells

B-type natriuretic peptide inhibits angiotensin II-induced proliferation and migration of pulmonary arterial smooth muscle cells

Dobutamine Therapy is Associated with Worse Clinical Outcomes Compared with Nesiritide Therapy for Acute Decompensated Heart Failure: A Systematic Review and Meta-Analysis

Reduced immunoreactivities of B-type natriuretic peptide in pulmonary arterial hypertension rats after ranolazine treatment

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