BNP (1-32), human, a biologically active 32 amino acid, contains a 17 amino acid disulfide ring and the linear 76 amino acid N-terminal peptide (NT), with cardiorenal protective properties[1]. BNP (1-32) binds to the natriuretic peptide type A receptor (NPR-A) and via the second messenger cyclic guanosine monophosphate (cGMP) mediates a variety of actions including vasodilation, natriuresis, suppression of renin secretion, lusitropism, and inhibition of fibrosis[2]. BNP (1-32) is widely used as a biomarker in the diagnosis and prognosis of heart failure and cardiovascular disease [3]. Intravenous infusion of a high dose of BNP (1-32) can lead to a significant increase in plasma free fatty acids[4].
References:
[1] Polak J, Kotrc M, Wedellova Z, et al. Lipolytic effects of B-type natriuretic peptide1–32 in adipose tissue of heart failure patients compared with healthy controls[J]. Journal of the American College of Cardiology, 2011, 58(11): 1119-1125.
[2] Boerrigter G, Costello-Boerrigter L C, Harty G J, et al. Des-serine-proline brain natriuretic peptide 3–32 in cardiorenal regulation[J]. American journal of physiology-Regulatory, integrative and comparative physiology, 2007, 292(2): R897-R901.
[3] Heublein D M, Huntley B K, Boerrigter G, et al. Immunoreactivity and guanosine 3′, 5′-cyclic monophosphate activating actions of various molecular forms of human B-type natriuretic peptide[J]. Hypertension, 2007, 49(5): 1114-1119.
[4] Bartels E D, Guo S, Kousholt B S, et al. High doses of ANP and BNP exacerbate lipolysis in humans and the lipolytic effect of BNP is associated with cardiac triglyceride content in pigs[J]. Peptides, 2019, 112: 43-47.