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Cardiac ACE2/angiotensin 1–7/Mas receptor axis is activated in thyroid hormone-induced cardiac hypertrophy
Author(s) -
Gabriela Placoná Diniz,
Nathalia Senger,
Marcela Sorelli CarneiroRamos,
Robson A.S. Santos,
Maria Luiza Morais BarretoChaves
Publication year - 2015
Publication title -
therapeutic advances in cardiovascular disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 33
eISSN - 1753-9455
pISSN - 1753-9447
DOI - 10.1177/1753944715623228
Subject(s) - medicine , cardiac hypertrophy , angiotensin ii , receptor , endocrinology , thyroid , angiotensin 1 , hormone , renin–angiotensin system , muscle hypertrophy , cardiology , blood pressure
Thyroid hormone (TH) promotes marked effects on the cardiovascular system, including the development of cardiac hypertrophy. Some studies have demonstrated that the renin-angiotensin system (RAS) is a key mediator of the cardiac growth in response to elevated TH levels. Although some of the main RAS components are changed in cardiac tissue on hyperthyroid state, the potential modulation of the counter regulatory components of the RAS, such as angiotensin-converting enzyme type 2 (ACE2), angiotensin 1-7 (Ang 1-7) levels and Mas receptor induced by hyperthyroidism is unknown. The aim of this study was to investigate the effect of hyperthyroidism on cardiac Ang 1-7, ACE2 and Mas receptor levels.

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