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Angiotensin‐(1–7) Prevents cardiovascular changes induced by hyperthyroidism
Author(s) -
Senger Nathalia,
Melo Marcos Barrouin,
Santos Maria José Campagnole,
Santos Robson Augusto,
BarretoChaves Maria Luiza Morais
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb642
Subject(s) - medicine , endocrinology , ejection fraction , angiotensin ii , cardiac function curve , muscle hypertrophy , renin–angiotensin system , cardiac hypertrophy , triiodothyronine , heart failure , thyroid , receptor , cardiology , blood pressure
High levels of thyroid hormone (TH) are commonly associated with cardiac hypertrophy and with a hyperdynamic heart condition. We previously demonstrated that cardiac hypertrophy induced by TH is mediated by Renin‐Angiotensin System (RAS) activation. In present study we tested the hypothesis that elevated circulating Angiotensin‐(1–7) levels attenuate the cardiovascular changes induced by TH. Wild Sprague‐Dawley (SD) or transgenic rats (TG) that constitutively overexpress an Angiotensin‐(1–7)‐producing fusion protein (TGR‐L3292) received daily injections (i.p.) of triiodothyronine (T3) (7μg/100g of body weight/day) for 14 days in order to develop hyperthyroidism. Cardiac hypertrophy was characterized and echocardiography experiments were performed to evaluate cardiac function parameters. The animals were handled according to National Institute of Health guidelines (NIH) – guide for the care and use of laboratory animals. Hyperthyroid wild‐type rats (SD‐T3) presented a significant increase in the cardiac mass, which was undetectable in the transgenic rats treated with T3 (TG‐T3). The administration of A779 (5μg/Kg/h), an antagonist of Angiotensin‐(1–7) receptor (Mas receptor), prevented the anti‐hypertrophic effect of Angiotensin‐(1–7) observed in TG‐T3. Echocardiography parameters showed that TG‐T3 rats exhibited a mitigation of the cardiac hyperdynamic condition observed in SD‐T3 rats, improving the following parameters: ejection fraction (EF%), fractional shortening (FS%), E/A ratio and heart rate. On the other hand, the treatment with A779 inhibited or attenuated the cardioprotective actions of Angiotensin‐(1–7) observed in TG‐T3. Collectively, these findings improve understanding of the cardiac hypertrophy observed in hyperthyroidism and may provide groundwork for the development of a new pharmacological strategy to the cardiac hyperdynamic condition observed in this disease. Support or Funding Information Foundation for the Support of Research in the State of São Paulo; [FAPESP #2013/16348‐6] and CNPq [National Council of Technological and Scientific Development].