Neuro-endocrine changes as new targets in the drug treatment of congestive heart failure

The classical therapy of congestive heart failure (CHF) with inotropic agents (digitalis and newer inotropics) and diuretic agents remains unsatisfactory in many cases. More recently it is recognized, that some of the neuro-endocrine compensatory processes associated with CHF are detrimental in the long run, and therefore potentially targets for drug treatment. This holds for the following neuro-endocrine mechanisms:o

1. 1)

   increased activity of the sympathetic nervous system and high plasma catecholamines, accompanied by down-regulation of β₁- but not β₂-receptors in the heart:

2. 2)

   stimulation of the renin-angiotensin-aldosterone system (RAAS), causing higher levels of renin, A II and aldosterone.

The detrimental sequelae of both processes are even enhanced by their complex mutual interactions. Drug treatment aiming to reduce or suppress these processes and their negative results is potentially offered by: vasodilators, counteracting vasoconstriction, low dose selective β₁-adrenoceptor blockers, which will not only impair tachycardia but also upregulate cardiac β₁-recep-