Natriuretic Peptide Deficiency—When There Is Too Little of a Good Thing

In 1981, de Bold et al¹ described a substance in rat atria that elicited a brisk natriuretic and diuretic response when infused into normal rats.¹ They subsequently isolated and purified this substance, calling it atrial natriuretic factor (it is now known as atrial natriuretic peptide [ANP]). The discovery of ANP and the closely-related B-type natriuretic peptide (BNP) established the important endocrine function of the heart. The natriuretic peptide hormones promote a variety of actions that reduce cardiac load including vasodilation, natriuresis, and inhibition of the renin-angiotensin-aldosterone system. Thus, via secretion of ANP and BNP, the heart contributes to the regulation of its own wall stress, as well as systemic blood pressure and salt homeostasis. A growing body of evidence also suggests that the natriuretic peptides have favorable effects on fat metabolism and glucose handling.²