c-type natriuretic peptide

C-type natriuretic peptide (CNP) is an endogenous peptide hormone primarily produced by the vascular endothelium, heart, and several endocrine glands. It is a member of the natriuretic peptide family, which also includes atrial natriuretic peptide (ANP) and brain (B-type) natriuretic peptide (BNP). Unlike ANP and BNP, which have strong diuretic and natriuretic effects, CNP mainly acts in a paracrine manner to regulate vascular tone and local blood flow. Its principal biological actions include vasodilation of arteries and veins, inhibition of vascular smooth muscle cell proliferation, reduction in leukocyte and platelet reactivity, prevention of atherogenesis and aneurysm formation, as well as modulation of cardiac structure and function. CNP exerts its effects primarily through activation of specific receptors—natriuretic peptide receptor B (NPR-B) for signaling functions and NPR-C for clearance—and has been shown to antagonize the renin-angiotensin-aldosterone system locally by inhibiting angiotensin-converting enzyme activity in blood vessels. While recombinant analogues or modified forms are under investigation for conditions such as achondroplasia due to their role in bone growth regulation, native CNP itself is not currently approved as a pharmaceutical drug but represents an important target for cardiovascular therapeutics[1][3][4][5][6].

Other names

CNP