Corin: an ANP protease that may regulate sodium reabsorption in nephrotic syndrome.
The serine/threonine protease corin, which proteolytically activates atrial natriuretic peptide (ANP), is reduced in the kidneys of animals with nephrotic syndrome and glomerular nephritis. Polzin et al. provide evidence for a linkage between the decreased corin and β-epithelial sodium channel, phosphodiesterase 5, and cGMP-dependent protein kinase II in the nephrotic kidney. They propose that decreases in cGMP resulting from the reduced corin may be responsible for the Na(+) retention and volume expansion that are hallmarks of these kidney diseases.
Klein
Janet D
JD
Department of Renal Medicine, Emory University, Atlanta, Georgia 30322, USA. jklei01@emory.edu
D000042:Absorption; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism; D006152:Cyclic GMP / Q000502:physiology; D054706:Cyclic Nucleotide Phosphodiesterases, Type 5 / Q000502:physiology; D006801:Humans; D009404:Nephrotic Syndrome / Q000378:metabolism*; D012697:Serine Endopeptidases / Q000502:physiology*; D012964:Sodium / Q000378:metabolism*
D009320:Atrial Natriuretic Factor; D012964:Sodium; D054706:Cyclic Nucleotide Phosphodiesterases, Type 5; C517382:Pde5a protein, mouse; C119812:CORIN protein, human; D012697:Serine Endopeptidases; D006152:Cyclic GMP