C-type natriuretic peptide (CNP) is a peptide produced by the vascular endothelium with vasodilative properties. It shares structural and physiological properties with the atrial and brain natriuretic peptides (ANP and BNP), whose central role in the pathophysiology of heart failure (CHF) is firmly established. The role of CNP, first isolated from porcine brain, has not been yet completely determined. The transcription of the gene, that in man is located on chromosome 2, is regulated by factors such as tumor necrosis factor and interleukin-1. Two mature forms of the peptide exist: CNP-53, that predominates in tissues and CNP-22, found mainly in plasma. As recently found, CNP is produced directly in the myocardium and an increase in plasma levels of this peptide and of its precursor was observed in CHF. The aim of this review was to examine the current literature relating to cardiovascular functions of CNP and in particular to its role in CHF. In fact, CNP may represent an important new local autocrine and endocrine mediator in CHF although further evaluations are required to define its full pathophysiological role in this disease.