Mas receptor blockade impairs exercise-induced cardiac hypertrophy

IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Peptides Pub Date : 2024-09-10 DOI:10.1016/j.peptides.2024.171296
Christoffer Novais de Farias Silva , Amanda de Sá Martins de Bessa , Jaqueline Moura da Costa , Paulo Ricardo Lopes , Ângela Ribeiro Neves , Monique Machado Louredo Teles Bombardelli , Diego Basile Colugnati , Gustavo Rodrigues Pedrino , Elizabeth Pereira Mendes , Robson Augusto Sousa dos Santos , Manoel Francisco Biancardi , Fernanda Cristina Alcantara dos Santos , Carlos Henrique Castro
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Abstract

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.

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Mas 受体阻断剂会损害运动诱导的心肌肥大
运动训练会导致生理性心脏肥大,而由血管紧张素转换酶 2、血管紧张素-(1-7)和 Mas 受体组成的肾素-血管紧张素系统保护轴似乎参与了这一过程。然而,Mas 受体的基础活性在运动诱导的生理性心脏肥大中的作用仍不清楚。我们评估了阻断 Mas 受体对接受跑步训练的大鼠左心室结构和功能的影响。大鼠被分为 4 组:静坐组(S)、静坐 + A-779(Mas 受体拮抗剂,120 微克/公斤/天,静注;SA)、训练组(60 分钟跑步机跑步训练,每周 5 天,8 周;T)和训练 + A-779 组(TA)。实验结束时,静坐大鼠和接受 A-779 治疗的大鼠收缩压较高。A-779 能阻止运动引起的左心室肥大,并增加久坐大鼠和训练大鼠的胶原沉积。SA 组心肌细胞的肌节长度和厚度增加,线粒体拉长,糖原沉积,肌质网蓄水池增大。TA 组的肌节厚度和细胞质减少,并出现退化现象。这些研究结果表明,Mas 受体的基础活性对心肌细胞外基质的正常周转和心肌细胞肉瘤结构的维持至关重要。
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来源期刊
Peptides
Peptides 医学-生化与分子生物学
CiteScore
6.40
自引率
6.70%
发文量
130
审稿时长
28 days
期刊介绍: Peptides is an international journal presenting original contributions on the biochemistry, physiology and pharmacology of biological active peptides, as well as their functions that relate to gastroenterology, endocrinology, and behavioral effects. Peptides emphasizes all aspects of high profile peptide research in mammals and non-mammalian vertebrates. Special consideration can be given to plants and invertebrates. Submission of articles with clinical relevance is particularly encouraged.
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