In contrast, physical training is generally followed by beneficial cardiomyocyte hypertrophy and reduction in the deposition of fibrotic tissue [19]. We speculate that a distinct expression pattern of Mas in cardiomyocytes Afatinib ic50 and cardiac fibroblasts might explain, at least in part, why physical training did not change the expression of Mas whereas chronic treatment with isoproterenol induced
a reduction in cardiac Mas expression. Next, we used DOCA-salt hypertensive rats and infarcted rats in which cardiac Mas expression was assessed at two different time frames. DOCA-salt rats presented a significant increase in cardiac function and cardiac hypertrophy after 4 and 6 weeks of treatment when compared to control rats. However, cardiac Mas expression in DOCA-salt rats was different from control
rats only after 6 weeks of treatment. This result is especially important as it shows that changes in cardiac function or structure are not always accompanied by changes in Mas expression levels. Nevertheless, it is plausible that Mas expression could decrease in DOCA rats with the progression of the disease. In fact, at the time frame investigated in this study DOCA rats were hypertensive with compensated Pictilisib concentration cardiac function, as shown by echocardiography measurements. In this way, evaluation of Mas expression at additional time-points is important in order to further understand the relationship between disease progression and expression of Mas in different experimental models. Since higher or lower levels of Mas expression do not necessarily represent gain or loss of receptor functional activity, it is of fundamental
importance to assess in future studies Mas functionality, as well as expression levels of ACE2 and Ang-(1-7). Finally, we assessed cardiac Mas expression at Nintedanib (BIBF 1120) 7 and 21 days post-infarction. Interestingly, at the early stage (7 days) cardiac Mas expression did not change when compared to sham group. However, at a later stage (21 days) cardiac Mas expression decreased significantly. In keeping with this finding, Ocaranza et al. [15] have shown that cardiac ACE2 activity decreases with the progression of cardiac disease. Importantly, in this study the authors have demonstrated that cardiac ACE2 activity increases after 1 week of cardiac infarction in rats, while at 8 weeks post injury infarcted rats presented a significant decrease in ACE2 activity when compared to control rats. Thus, these results suggest that ACE2/Ang-(1-7) is generally elevated at the beginning of the establishment of the cardiovascular disease, possibly as an attempt of limiting the damage, while it is depressed in the late phase of disease. In agreement, our study shows that Mas expression levels were altered mainly at a later stage.
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