The Renin-Angiotensin-Aldosterone System and the Sympathetic Nervous System in Congestive Heart Failure: Mutual Interactions Between Both Systems

Abstract

Congestive heart failure is frequently accompanied by complex compensatory mechanisms, involving, among others, the peripheral sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). In many cases the reflex stimulation of these mechanisms is detrimental in the long term, although initially such mechanisms may be at least of symptomatic benefit to the patient. A renewed interest in the reflex compensation mechanisms has developed upon introduction of inhibitors of the angiotensin-converting enzyme (ACE) inhibitors captopril and enalapril in the treatment of congestive heart failure. The major therapeutic activity of ACE inhibitors is undoubtedly based upon vasodilatation and, hence, unloading of the heart. However, it could be imagined that an additional action of such drugs on the aforementioned reflex mechanism somehow contributes to the symptomatic improvement of the syndrome of congestive heart failure. This situation is made even more complex by the obvious interaction between the sympathetic nervous system (SNS) and the RAAS, the two major systems involved in the sequelae of congestive heart failure and its therapy with ACE inhibitors. Before discussing this interaction, it would seem useful to briefly review the pathophysiological changes induced by congestive heart failure in each system separately.