C‐Type Natriuretic Peptide Inhibits Intimal Thickening after Vascular Injury

C-type natriuretic peptide (CNP) suppresses plasminogen activator inhibitor-1 (PAI-1) in vivo

“…CNP infused directly into the carotid artery under the collar would have spilled over to the ipsilateral collared artery, albeit at a much reduced concentration, and this may have been sufficient to prevent the collar-induced increase in endothelial PAI-1. Previous studies by others investigating the effects of CNP on neointimal formation in vivo used systemic infusions of CNP at the quite high dose of 1 Ag/kg/min (or~30 nmol/kg/h) [10,37,38]. This was~1000-fold higher than the dose of 100 pmol/rabbit/h (or~30 pmol/kg/h) employed in our present study.…”

Urinary C-type natriuretic peptide excretion: a potential novel biomarker for renal fibrosis during aging

“…Studies have increasingly supported a fibro-inhibiting role for CNP/NPR-B signaling in terms of both suppressing collagen production and reducing cell proliferation. Particularly, in vivo studies have reported that exogenous CNP inhibited myofibroblast proliferation and activation (6,34), prevented neointimal formation and thickening after arterial injury (12,35), and suppressed post-acute myocardial infarction-induced cardiac fibrosis (30). Furthermore, in vitro studies have demonstrated that CNP possesses robust antifibrotic and antiproliferative properties in young rat and adult human cardiac fibroblasts (16,29).…”

Cardioprotective actions of peptide hormones in myocardial ischemia

“…However, CNP mRNA has been confirmed in normal rat atrial and ventricular extracts [31] and there is accumulating evidence that myocardial CNP expression may increase under pathological conditions, notably during heart failure and remodelling [32,33]. It has been proposed that the peptide may exert autocrine/paracrine functions in regulating coronary vascular tone as well as modulation of cell growth [24,34,35].…”