Mas receptor blockade impairs exercise-induced cardiac hypertrophy

• Published in: Peptides (New York, N.Y. : 1980) Vol. 181; p. 171296
• Main Authors: Silva, Christoffer Novais de Farias, Bessa, Amanda de Sá Martins de, Costa, Jaqueline Moura da, Lopes, Paulo Ricardo, Neves, Ângela Ribeiro, Teles Bombardelli, Monique Machado Louredo, Colugnati, Diego Basile, Pedrino, Gustavo Rodrigues, Mendes, Elizabeth Pereira, Santos, Robson Augusto Sousa dos, Biancardi, Manoel Francisco, Santos, Fernanda Cristina Alcantara dos, Castro, Carlos Henrique
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.11.2024
• Subjects: Angiotensin-(1−7); Cardiac hypertrophy; Exercise; Fibrosis; Renin-angiotensin system; Cardiac hypertrophy; Angiotensin-(1−7); Exercise; Renin-angiotensin system; Fibrosis; exercise; fibrosis; cardiac hypertrophy; Angiotensin-(1-7); renin-angiotensin system
• ISSN: 0196-9781; 1873-5169; 1873-5169
• DOI: 10.1016/j.peptides.2024.171296

Exercise training leads to physiological cardiac hypertrophy and the protective axis of the renin-angiotensin system composed of angiotensin-converting enzyme 2, angiotensin-(1–7), and Mas receptor seems involved in this process. However, the role of the basal activity of the Mas receptor in exercise-induced physiological cardiac hypertrophy is still unclear. We evaluated the effects of the Mas receptor blockade on the left ventricular structure and function of rats submitted to running training. Rats were assigned to 4 groups: sedentary (S), sedentary + A-779 (Mas receptor antagonist, 120 µg/kg/day, i.p.; SA), trained (60-minute treadmill running sessions, five days a week, 8 weeks; T), and trained + A-779 (TA). Systolic blood pressure was higher in sedentary and trained rats treated with A-779 at the end of the experimental period. The A-779 treatment prevented the left ventricular hypertrophy evoked by physical exercise and increased collagen deposition in sedentary and trained rats. Cardiomyocytes from the SA group presented increased length and thickness of the sarcomeres, elongated mitochondria, glycogen deposits, and enlarged cisterns of the sarcoplasmic reticulum. TA group presented a reduced sarcomere thickness and cytoplasm with a degenerative aspect. These findings show that the basal activity of the Mas receptor is essential for the proper turnover of the extracellular matrix in the myocardium and the maintenance of the sarcomeric structure of cardiomyocytes. [Display omitted] •Mas receptor is important for the proper development of exercise-induced cardiac hypertrophy.•Mas receptor blockade impairs the extracellular matrix deposition in trained rat hearts.•Mas receptor blockade generated a pathological profile in cardiomyocytes from trained rats.