ArticleFrontiers in physiology2015
Effect of Angiotensin(1-7) on Heart Function in an Experimental Rat Model of Obesity.
Article in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- A Retrospective Study to Investigate the Relationship Between Body Mass Index and Hemodynamic Characteristics in Hypertensive Patients.Journal of clinical hypertension (Greenwich, Conn.) · 2025Review
- Increase in body weight is lowered when mice received fecal microbiota transfer from donor mice treated with the ATFrontiers in pharmacology · 2024Article
- PDZK1 improves ventricular remodeling in hypertensive rats by regulating the stability of the Mas receptor.Amino acids · 2023Article
- Mas receptor: a potential strategy in the management of ischemic cardiovascular diseases.Cell cycle (Georgetown, Tex.) · 2023Review
- The AT1 Receptor Blocker Telmisartan Reduces Intestinal Mucus Thickness in Obese Mice.Frontiers in pharmacology · 2022Article
- Targeting the Protective Arm of the Renin-Angiotensin System to Reduce Systemic Lupus Erythematosus Related Pathologies in MRLFrontiers in immunology · 2020Article
- The antiobese effect of AT1 receptor blockade is augmented in mice lacking Mas.Naunyn-Schmiedeberg's archives of pharmacology · 2019Article
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Authors and funding
7 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aimObesity is a risk factor for the development of cardiovascular diseases. Recently it was shown that overexpression of the Mas-receptor antagonist angiotensin(1-7) could prevent from diet-induced obesity. However, it remained unclear whether diet-induced obesity and angiotensin(1-7) overexpression might also have effects on the cardiovascular system in these rats.
methodsTwenty three male Sprague Dawley rats were fed with standard chow (SD+chow, n = 5) or a cafeteria diet (SD+CD, n = 6) for 5 months. To investigate the effect of angiotensin(1-7) transgenic rats, expressing an angiotensin(1-7)-producing fusion protein in testis were used. These transgenic rats also received a 5 month's feeding period with either chow (TGR+chow, n = 6) or cafeteria diet (TGR+CD, n = 6), respectively. Hemodynamic measurements (pressure-volume loops) were carried out to assess cardiac function and blood pressure. Subsequently, hearts were explanted and investigated according to the Langendorff technique. Furthermore, cardiac remodeling in these animals was investigated histologically.
resultsAfter 5 months cafeteria diet feeding rats showed a significantly increased body weight, which could be prevented in transgenic rats. However, there was no effect on cardiac performance after cafeteria diet in non-transgenic and transgenic rats. Moreover, overexpression of angiotensin(1-7) deteriorated cardiac contractility as indicated by impaired dp/dt. Furthermore, histological analysis revealed that cafeteria diet led to myocardial fibrosis in both, control and transgenic rats and this was not inhibited by an overproduction of angiotensin(1-7).
conclusionThese results indicate that an overexpression of circulating angiotensin(1-7) prevents a cafeteria diet-induced increase in body weight, but does not affect cardiac performance in this experimental rat model of obesity. Furthermore, overexpression of angiotensin(1-7) alone resulted in an impairment of cardiac function.
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