title: The renal and cardiovascular effects of natriuretic peptides.
abstract: The landmark report by de Bold et al. in 1981 signified the heart as one of the endocrine organs involved in fluid and salt balance (de Bold AJ, Borenstein HB, Veress AT, Sonnenberg H.Life Sci28: 89-94, 1981). Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are secreted from cardiomyocytes in response to cardiac stretch as in the case of heart failure, whereas C-type natriuretic peptide (CNP) is secreted from endothelial and renal cells in response to cytokines and endothelium-dependent agonists, such as acetylcholine. Binding ANP or BNP to natriuretic peptide receptor A induces cyclic guanylyl monophosphate as second messenger in the target cells to mediate the following: natriuresis; water diuresis; increasing glomerular filtration rate; decreasing systemic sympathetic activities; plasma volume; cardiac output and blood pressure; and curbing mitoses of heart fibroblasts and hypertrophy of cardiovascular muscle cells. ANP, BNP, and CNP are cleared from the bloodstream by natriuretic peptide receptor C and degraded by an ectoenzyme called neprilysin (NEP). The plasma levels of BNP are typically >100 pg/ml in patients with congestive heart failure. Sacubitril/valsartan is an angiotensin receptor NEP inhibitor that prevents the clinical progression of surviving patients with heart failure more effectively than enalapril, an angiotensin-converting enzyme inhibitor. A thorough understanding of the renal and cardiovascular effects of natriuretic peptides is of major importance for first-year medical students to gain insight into the significance of plasma levels of BNP in patients with heart failure.
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Jinan University, Guangzhou, China.
authors.forename: Philip Ching Yat
authors.initials: PC
authors.lastname: Wong
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Jinan University, Guangzhou, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Guo
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Jinan University, Guangzhou, China zad9017@gmail.com.
authors.forename: Aidong
authors.initials: A
authors.lastname: Zhang
mesh_terms: D000613:Aminobutyrates / Q000627:therapeutic use; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000378:metabolism; D001713:Biphenyl Compounds; D018450:Disease Progression; D004338:Drug Combinations; D004656:Enalapril / Q000627:therapeutic use; D006333:Heart Failure / Q000097:blood* / Q000188:drug therapy; D006801:Humans; D007668:Kidney / Q000503:physiopathology; D020097:Natriuretic Peptide, Brain / Q000097:blood / Q000378:metabolism; D020098:Natriuretic Peptide, C-Type / Q000097:blood / Q000378:metabolism; D045265:Natriuretic Peptides / Q000097:blood* / Q000378:metabolism*; D013777:Tetrazoles / Q000627:therapeutic use; D000068756:Valsartan
chemical_list: D000613:Aminobutyrates; D001713:Biphenyl Compounds; D004338:Drug Combinations; D045265:Natriuretic Peptides; D013777:Tetrazoles; D020097:Natriuretic Peptide, Brain; D020098:Natriuretic Peptide, C-Type; D004656:Enalapril; D000068756:Valsartan; D009320:Atrial Natriuretic Factor; C549068:sacubitril and valsartan sodium hydrate drug combination
keywords: ANP; BNP; CNP; atrial natriuretic peptide; natriuresis; natriuretic peptide receptors