Angiotensin-(1-7) Treatment Early in Life Prevents Cardiac Hypertrophy in Adult Hypertensive Rats.
Carolina Nobre Ribeiro PontesAmanda de Sá Martins de BessaLarissa Matuda MacedoMarcos Divino Ferreira-JuniorKeilah Valéria Naves CavalcanteHericles Mesquita CamposVanessa Rafaela Milhomem Cruz-LeiteÂngela Ribeiro NevesRodrigo Mello GomesPaulo César GhediniManoel Francisco BiancardiElizabeth Pereira MendesClayton Luiz BorgesGustavo Rodrigues PedrinoCarlos Henrique de CastroPublished in: Journal of cardiovascular pharmacology (2024)
Angiotensin (Ang)-(1-7) is a cardioprotective peptide of the renin-angiotensin system. Prepuberty has been considered as a later susceptible window of development, and stressful factors in this life phase can induce chronic diseases in adulthood. We aimed to investigate whether the treatment with Ang-(1-7) during the prepuberty could attenuate the development of hypertension and cardiac injury in adult spontaneously hypertensive rats (SHRs). SHRs were treated with Ang-(1-7) (24 μg/kg/h) from age 4 to 7 weeks. Systolic blood pressure was measured by tail-cuff plethysmography up to 17th week. Thereafter, echocardiography was performed, and the rats were euthanized for the collection of tissues and blood. Ang-(1-7) did not change the systolic blood pressure but reduced the septal and posterior wall thickness, and cardiomyocyte hypertrophy and fibrosis in SHR. In addition, Ang-(1-7) reduced the gene expression of atrial natriuretic peptide and brain natriuretic peptide, increased the metalloproteinase 9 expression, and reduced the extracellular signal-regulated kinases 1/2 phosphorylation. Ang-(1-7) also prevented the reduction of Mas receptor but did not change the protein expression of angiotensin-converting enzyme, angiotensin-converting enzyme 2, AT1, and AT2. The treatment with Ang-(1-7) decreased the malondialdehyde (MDA) levels and increased superoxide dismutase-1 and catalase activities and protein expression of catalase. Our findings demonstrate that the treatment of SHR with Ang-(1-7) for 3 weeks early in life promotes beneficial effects in the heart later in life, even without altering blood pressure, through mechanisms involving the reduction of oxidative stress and ERK1/2 phosphorylation. In addition, this study supports the prepuberty as an important programming window.
Keyphrases
- angiotensin ii
- angiotensin converting enzyme
- blood pressure
- gene expression
- left ventricular
- oxidative stress
- heart failure
- hypertensive patients
- heart rate
- dna damage
- signaling pathway
- poor prognosis
- computed tomography
- multiple sclerosis
- hydrogen peroxide
- cell proliferation
- combination therapy
- transcription factor
- cell death
- adipose tissue
- study protocol