Angiotensin-converting Enzyme Inhibition and Angiotensin Receptor Blockade

Activation of the renin-angiotensin-aldosterone system is one of the predominant abnormalities of heart failure. The degree of increase in plasma renin activity provides an indicator for prognosis in heart failure patients [1]. Patients with mild and asymptomatic heart failure demonstrate relatively less activation, but even these values are increased compared with normal. The degree of renin activity is intensified in the presence of diuretic therapy. Angiotensin II causes constriction of the systemic vasculature and causes vasoconstriction of both the afferent and efferent renal arterioles. In some patients with severe heart failure, treatment with angiotensin-converting enzyme (ACE) inhibitors may cause a deterioration of renal function. This may be related to fixed renal artery disease, or alternatively from selective blocking of the constrictor action of angiotensin II on the efferent arteriole [2]. Renin system components have been identified in the myocardium and vasculature, where they adversely affect fibrosis and remodeling, as well as cellular dysfunction. These findings suggest that the renin-angiotensin-aldosterone system has effects on cardiac function beyond altering sodium excretion and cardiac afterload. Not only is angiotensin II a potent vasoconstrictor, but it causes a direct effect on hypertrophy of myocytes, and may lead to energy supply mismatch as the capillary bed perfuses a larger bed [3].