Compensatory changes of sympathetic tone, the renin-angiotensin-aldosterone system, vasopressin, and ANF as potential therapeutic targets in congestive heart failure.

Congestive heart failure (CHF) is not only reflected by such mechanical problems as forward- and backward failure, but it is also associated with a complex pattern of compensatory neuro-endocrine mechanisms, e.g., enhanced activity of both the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS); enhanced release of vasopressin from the pituitary gland; enhanced release of the atrial natriuretic factor (ANF) from the cardiac atria. These neuro-endocrine mechanisms not only operate as such but also display a complex pattern of mutual interactions. These mechanisms, though potentially beneficial short-term, may also be harmful when persisting during progression of the disease. For this reason they offer potential targets in the treatment of CHF besides the classical measures aimed directly at improving cardiac contractility. The following groups of drugs are discussed as therapeutic measures that suppress the aforementioned detrimental compensatory mechanisms: various types of vasodilator drugs; diuretics; beta 1-adrenoceptor blocking agents in low dosage; saralasin; ACE-inhibitors. So far, the enhanced release of vasopressin and ANF have not offered realistic new therapeutic targets in CHF, although their pathophysiologic issue is highly relevant.