Beneficial effects of CNP chronic administration on vascular proinflammatory and profibrotic cytokines expression in spontaneously hypertensive rats

CANIFFI, CAROLINA; GÓMEZ, MARTÍN; ALCOBER, LUCÍA; ALADRO, MANUELA; GONZÁLEZ MAGLIO, DANIEL; TOBLLI, JORGE; ARRANZ, CRISTINA

Buenos Aires

Congreso; II International Congress in Translational Medicine. International Master Program in Biomedical Sciences; 2015

Universidad de Buenos Aires y University of Friburg

Growing evidence shows that the expression and release of a number of inflammatory cytokines are increased in hypertension and are also present at sites of cardiovascular fibrosis. In fact, many of these inflammatory mediators are responsible for the activation of collagen producing fibroblasts. In addition, proinflammatory cytokines such as tumoral necrosis factor-alpha (TNFα) and interleukin-1 (IL-1) stimulate the release of Ctype natriuretic peptide (CNP), showing a potential role of CNP as a modulator of the inflammatory process.Aim: evaluate the effects of CNP chronic treatment on vascular fibrosis and its inflammatory state in spontaneously hypertensive rats (SHR).Design and method: 12-week-old male SHR were infused with CNP (0.75 μg/hr) or saline (S) (osmotic pumps, 14 days). Systolic blood pressure (SBP, mmHg) was recorded by tailcuff method. After treatment, animals were decapitated and the thoracic aorta artery (AA) was extracted to determine: fibrosis (collagen % by Picrosiriusred stain), transforming growth factor-beta1 (TGF-β1) and Smad (% stained area by immunohistochemistry (IHC)) and inflammation parameters (IL-6 and TNF-α, aorta % positive stain/mm2 by IHC and IL-1β, pg/mg protein by ELISA). Statistics: t test; n=6 rats/group.Results: SBP: S= 183±3, CNP= 159±5**; Collagen: S=34.7±3.5, CNP=19.8±1.7**; TGF- β1: S= 25.1±0.7, CNP= 18.5±0.6*; Smad: S= 6.1±0.7, CNP= 2.7±0.4**; IL-6 SHR: S=19.2±0.8, CNP=3.4±0.6**; TNF-α SHR: S= 18.5±0.9, CNP=4.4±0.7**; IL-1β SHR: S= 1.9±0.2, CNP= 1.4±0.1**. Values are means ± SEM. *p