C-type natriuretic peptide prevents angiotensin II-induced cardiac remodelling and dysfunction

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.

• Publication year

  2015

• Venue

  BMC Pharmacology and Toxicology

• Publication date

  2015-09-02

• Fields of study

  Medicine

• Identifiers
  DOI 10.1186/2050-6511-16-S1-A78PMCID 4565488
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

• No claims are published for this paper.

• No concepts are published for this paper.

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