Hormone used in regulating the cardiovascular system
Natriuretic peptide-binding receptors and ligand selectivity.[1]
A natriuretic peptide is a hormone molecule that plays a crucial role in the regulation of the cardiovascular system. These hormones were first discovered in the 1980s and were found to have very strong diuretic, natriuretic, and vasodilatory effects. There are three main types of natriuretic peptides: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP).[1] Two minor hormones include Urodilatin (URO) which is processed in the kidney and encoded by the same gene as ANP, and Dendroaspis NP (DNP) that was discovered through isolation of the venom from the green mamba snake.[2] Since they are activated during heart failure, they are important for the protection of the heart and its tissues.[1]
Additionally, there are three natriuretic peptide receptors: Natriuretic Peptide Receptor-A (NPR-A), Natriuretic Peptide Receptor-B (NPR-B), and Natriuretic Peptide Receptor-C (NPR-C). NPR-A and NPR-B use cyclic guanosine monophosphate (cGMP) as its intracellular messenger. NPR-A binds selectively to ANP and BNP while NPR-B binds selectively to CNP.[1] Although initially thought to have no signaling activity, NPR-C is now believed to inhibit cyclic adenosine monophosphate (cAMP) using the Giα subunit along with activating phospholipase C-β using the Giβγ subunit. The three natriuretic peptides ANP, BNP, and CNP can bind to NPR-C however it has a higher affinity towards ANP and CNP. Natriuretic peptides will lose their activity when degraded by the enzyme neprilysin which is found on the plasma membrane.[1]
^ abcdeKuwahara, Koichiro (2021-11-01). "The natriuretic peptide system in heart failure: Diagnostic and therapeutic implications". Pharmacology & Therapeutics. 227: 107863. doi:10.1016/j.pharmthera.2021.107863. ISSN 0163-7258.
^Sangaralingham, S Jeson; Kuhn, Michaela; Cannone, Valentina; Chen, Horng H; Burnett Jr, John C (25 August 2022). "Natriuretic peptide pathways in heart failure: further therapeutic possibilities". Cardiovascular Research. 118 (18): 3416–3433 – via Oxford Academic.
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