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Cardiac morphological and functional changes induced by C-type natriuretic peptide are different in normotensive and

Carolina Caniffi1,2, Estefanía Prentki Santos1,2, Flavia M Cerniello1,2

  • 1Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Ciencias Biológicas, Cátedra de Fisiología.

Journal of Hypertension
|July 11, 2020
PubMed

Insights

Chronic C-type natriuretic peptide (CNP) treatment reduces cardiac inflammation and fibrosis in hypertensive rats. This cardiovascular protective factor attenuates hypertension and end-organ damage, improving heart function.

Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Pathology

Background:

  • Inflammation and fibrosis are key drivers of cardiovascular remodeling.
  • C-type natriuretic peptide (CNP) is an endothelium-derived factor with known cardiovascular protective roles.
  • The in-vivo effects of CNP on hypertension-linked cardiac remodeling remain under-investigated.

Purpose of the Study:

  • To investigate the effects of chronic CNP administration on cardiac inflammatory and fibrotic mechanisms.
  • To assess CNP's impact on cardiovascular remodeling in normotensive and spontaneously hypertensive rats (SHR).

Main Methods:

  • Twelve-week-old male SHR and normotensive rats received continuous infusion of CNP or saline for 14 days.
  • Echocardiograms, electrocardiograms, and systolic blood pressure (SBP) were measured.
  • Cardiac tissue analysis included inflammatory/fibrotic markers, nitric oxide (NO) system activity, and oxidative damage.

Main Results:

  • SHR exhibited lower cardiac output, left ventricular fibrosis/hypertrophy, higher NO activity, and increased oxidative damage compared to normotensive rats.
  • Chronic CNP treatment attenuated hypertension and ventricular hypertrophy in SHR, without affecting normotensive rats.
  • CNP reduced pro-inflammatory and pro-fibrotic markers, oxidative damage, and collagen content, while upregulating the NO system in SHR.

Conclusions:

  • Chronic CNP treatment effectively attenuates hypertension and associated cardiac end-organ damage.
  • CNP exerts anti-inflammatory and anti-fibrotic effects in the heart.
  • The findings highlight CNP's potential as a therapeutic agent for hypertension-related cardiovascular remodeling.
Abstract

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