As heart failure sets in, there is activation of RAS (Fig 2.1). Adrenergic stimulation of beta-1 receptors in juxtaglomerular apparatus of the kidneys results in release of renin. Another mechanism i.e. responsible for renin release is baroreceptor stimulation in renal vascular bed by reduction of renal blood flow.  

Angiotensin II that is released is a powerful vasoconstrictor and stimulates the release of aldosterone. It also causes remodeling of cardiac myocytes. Aldosterone retains sodium and has direct effects on myocardium. The result is increased systemic vascular resistance and development of edema. Hence the interruption of this renin-angiotensin-aldosterone axis by angiotensin-converting enzyme inhibitors (ACE-Inhibitors) or angiotensin receptor blockers (ARBs) has salutary effects as there is reduction in systemic vascular resistance, afterload reduction, mild diuresis and improvement in the cardiac output.

Angiotensin II also has direct role in modifying the structure and function of myocardium.