Mas receptor blockade impairs exercise-induced cardiac hypertrophy.

Autor: Silva CNF; Department of Physiological Sciences, Federal University of Goiás, Goiânia, GO, Brazil., Bessa ASM; Department of Physiological Sciences, Federal University of Goiás, Goiânia, GO, Brazil., Costa JMD; Department of Physiological Sciences, Federal University of Goiás, Goiânia, GO, Brazil., Lopes PR; Department of Physiological Sciences, Federal University of Goiás, Goiânia, GO, Brazil., Neves ÂR; Department of Physiological Sciences, Federal University of Goiás, Goiânia, GO, Brazil., Teles Bombardelli MML; Department of Physiological Sciences, Federal University of Goiás, Goiânia, GO, Brazil., Colugnati DB; Department of Physiological Sciences, Federal University of Goiás, Goiânia, GO, Brazil., Pedrino GR; Department of Physiological Sciences, Federal University of Goiás, Goiânia, GO, Brazil., Mendes EP; Department of Physiological Sciences, Federal University of Goiás, Goiânia, GO, Brazil., Santos RASD; Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil., Biancardi MF; Department of Histology, Embryology and Cell Biology, Federal University of Goiás, Goiânia, GO, Brazil., Santos FCAD; Department of Histology, Embryology and Cell Biology, Federal University of Goiás, Goiânia, GO, Brazil., Castro CH; Department of Physiological Sciences, Federal University of Goiás, Goiânia, GO, Brazil. Electronic address: castro@ufg.br.
Jazyk: angličtina
Zdroj: Peptides [Peptides] 2024 Nov; Vol. 181, pp. 171296. Date of Electronic Publication: 2024 Sep 10.
DOI: 10.1016/j.peptides.2024.171296
Abstrakt: 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.
Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
Externí odkaz: