Angiotensin II Requires an Intact Cardiac Thyrotropin-Releasing Hormone (TRH) System to Induce Cardiac Hypertrophy in Mouse.

SCHUMAN, MARIANO LUIS; PIROLA, CARLOS JOSÉ; AISICOVICH, MAIA; LANDA, MARIA SILVINA; PERES DIAZ, LUDMILA; TOBLLI, JORGE E.; GARCIA, SILVIA INES

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY

ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD

Año: 2018 vol. 114 p. 1 - 11

0022-2828

Cardiac tyhrotropin-releasing hormone (TRH) is overexpressed in the hypertrophied left ventricle (LV) of spontaneously hypertensive rats (SHR) and its inhibition prevents both hypertrophy and fibrosis. In a normal heart, the TRH increase induces fibrosis and hypertrophy opening the question of whether TRH could be a common mediator of left ventricular hypertrophy (LVH). We used angiotensin II (AngII) as an inductor of LVH to evaluate if the blockade of LV-TRH prevents hypertrophy and fibrosis in mice. We challenged C57BL/6 adult male mice with an infusion of AngII (osmotic pumps; 2 mg/kg.day) to induce LVH. Groups of mice were injected with an intracardiac siRNA-TRH or scrambled siRNA (siRNA-Con). Body weight, water intake and systolic arterial blood pressure (SABP) were measured daily. AngII significantly increased water intake and SABP (p