Endocrine Abstracts

Our group studies the influence of different endocrine factors on cardiovascular function. Ang II is the main vasopeptide of Renin-Angiotensin System (RAS) and exerts its potent biological effects through AT1 and AT2 receptors. In heart, Ang II induces cardiomyocyte hypertrophy and fibroblast hyperplasia through TGF-β1 recruitment. On the other hand, cardiovascular system is very sensitive to the action of the Thyroid Hormones (THs). One major cardiovascular manifestation of THs excess is cardiac hypertrophy. There is a long time our group contributes with different studies demonstrating the interaction between these endocrine systems (RAS and THs). Then, some manifestations that disrupt this interaction may help to explain the variability of cardiovascular manifestations observed, for example, in hypo and hyperthyroidism. In recent years, cardiac hypertrophy and remodeling have increasingly been documented as a consequence of activation of immunologic machinery, where recurrent or sustained inflammatory response plays a causal role in the development of hypertrophy and its transition to heart failure. We have identified novel pathways regulated by THs, which are related to the immune-inflammatory context and may potentially play important roles in the hyperthyroid heart. In this context and consistent with our findings, crosstalk between THs and the RAS suggests that the RAS may be an important mediator of some cardiovascular manifestations of THs. To address this question we have used in vivo and in vitro experimental models providing a suitable system to monitor changes in the structure and cardiovascular function induced by endocrine factors. Different methodologies have been employed and morphologic, morphometric, biochemical and functional parameters have been used to study molecular and cellular mechanisms associated to cardiovascular biology and in special to this endocrine interaction (RAS and THs).