Key result
Low-dose CNP prevents Angiotensin II-induced cardiac remodeling and improves LV contractility in mice.
Why the study?
Does synthetic C-type natriuretic peptide (CNP) prevent Angiotensin II-induced cardiac fibrosis and hypertrophy in vivo?
Does synthetic C-type natriuretic peptide (CNP) prevent Angiotensin II-induced cardiac fibrosis and hypertrophy in vivo?
This study aimed to investigate the potential of synthetic C-type natriuretic peptide to prevent Angiotensin II-induced cardiac remodeling in vivo.
Background Hypertensive cardiac remodelling is a major risk factor for cardiovascular morbidity and a leading cause of chronic heart failure. The activation of the renin-angiotensin system plays an important pathophysiological role in hypertensive cardiac remodelling [1]. C-type natriuretic peptide (CNP) belongs to the natriuretic peptide family. In the cardiovascular system, CNP is secreted from endothelial cells and possibly from cardiac fibroblasts, to act as autocrine/paracrine hormone [2]. It activates the guanylyl cyclase B (GC-B) receptor which synthesizes the second messenger cGMP. In vitro the CNP/GC-B pathway inhibits the proliferation and collagen synthesis of cardiac fibroblasts [3]. Therefore, we aimed to study the cardiac effects of synthetic CNP on Angiotensin II (Ang II)-induced cardiac fibrosis and hypertrophy in vivo.
No takes yet. Share an insight, caveat, or question.
Roloff et al. (2015) studied Angiotensin II-induced cardiac remodelling and dysfunction (n=48). C-type natriuretic peptide (CNP) vs. Vehicle (saline) or Angiotensin II alone was evaluated on Cardiac hypertrophy and fibrosis (LV weight/BW, myocyte diameters, interstitial fibrosis, BNP mRNA). Infusion of a low dose of C-type natriuretic peptide (CNP) largely prevented the deleterious structural cardiac changes and improved LV contractility induced by Angiotensin II in mice, independent of blood pressure.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: