In congestive heart failure, increased secretion of atrial natriuretic
peptide (ANP) is an important compensatory mechanism that unloads the
failing heart and promotes renal salt and water excretion. However, a
ctivation of opposing sodium-retaining factors, particularly the renin
-angiotensin system, reduces renal responsiveness to ANP and shifts th
e cardiovascular system to a state of decompensation.