This chapter aims to introduce the role of miRNAs in regulating neurohormonal activation. The natural
progression of heart failure is accompanied by the compensatory activation of cardiac and extracardiac
neurohormonal systems and changes in the anatomy and function of the left ventricle. An array of biologically
active molecules belong to the sympathetic adrenergic nervous system (norepinephrine) and renin–angiotensin–
aldosterone system (RAS) (Ang II and aldosterone), which are responsible for maintaining cardiac output through
increased retention of salt and water, peripheral arterial vasoconstriction, and contractility, as well as
inflammatory mediators that are responsible for cardiac repair and remodeling. Although, the role of miRNAs in
regulating the components of RAS and the adrenergic system is still poorly not well understood, several recent
observations are worth noting. In particular, miR-155 is implicated in suppressing the levels of the Ang II type 1
receptor, and miR-21 can increase aldosterone secretion in human adrenal cells. This chapter describes very
limited information in this regard.
