Myocardial pump deficiency is regarded to be the hemodynamic hallmark of 
congestive heart failure. A decline of arterial pressure in the systemic 
circulation is counter-regulated by vasoconstriction in the arteriolar vascular 
bed; the compensatory vasoconstriction, however, results in an increased 
afterload that in turn aggravates myocardial pump deficiency. As part of the 
counterregulatory systems the sympathetic nervous system is activated (increase 
of neuronal activity, increased plasma norepinephrine) and the 
renin-angiotensin-aldosterone system is stimulated as well (increased plasma 
renin activity, elevated angiotensin II serum levels, hyperaldosteronism). In 
parallel, serum levels of antidiuretic hormone (ADH) is despite a serum 
hypoosmolarity increased and only poorly compensated by release of the atrial 
natriuretic peptide. On the cellular level, congestive heart failure leads to a 
shift of the expression of contractile proteins towards to fetal forms (for 
instance myosin-isoenzymes). Although the counterregulatory activation of the 
neuroendocrine systems vasoconstricts the peripheral arteries thereby 
maintaining perfusion of vital organs, the rise in afterload ultimately leads to 
a progression of congestive heart failure. Consequently, vasodilators (such as 
ACE-inhibitors) that not only induce vasodilation in the peripheral arteries, 
but also inhibit progressive neuroendocrine stimulation evolved as excellent 
compounds for treating congestive heart failure.