**8. Thyroid hormones**

Thyroid hormones are stimulated by TSH anterior pituitary secretion. There is many actions of thyroid hormones on cardiovascular system exerted mainly by triiodothyronine (T3). These effects can be divided into genomic and extragenomic actions. T3 bounds to the nuclear receptors and activates many gens corresponding to key myocardial functions: myosin heavy chain (MHC), sarcoplasmic reticulum Caţţ-ATPase (SERCA2) and its inhibitor phospholamban (affecting cardiac contractile function and diastolic relaxation), voltage-gated Kţ channels, b1-adrenergic receptor, guanine nucleotide regulatory proteins, adenylate cyclase, NAţ/Kţ-ATPase, and Na/Ca exchanger. The main cardiovascular effects of T3 are: increased cardiac contractility, reduction of afterload, reduction of vascular resistance, chronotropic effect (increased heart rate), increases sodium reabsorption and water improves atrial filing pressure. All of this increase cardiac output.

T3 has genomic effects that maintain endothelial integrity, such as angiotensin receptors in vascular smooth muscle cells (VSMC). This supports the hypothesis that the vasculature is a principal target for T3 action. T3 decreases resistance in peripheral arterioles. Extragenomic actions include: modulation of cellular metabolic activities, such as glucose and amino acid transport, ion fluxes at the level of the plasma membrane, and mitochondrial gene expression and function.
