title: Atrionatriuretic peptide transforms cardiac sodium channels into calcium-conducting channels.
abstract: The atrionatriuretic peptide (ANP) is released from atrial cells in response to increased extracellular fluid volume and reduces sodium absorption by the kidney, thus reducing the blood volume. In this report, ANP suppressed the calcium and sodium currents in rat and guinea pig ventricular myocytes. The suppression of sodium current was caused by enhanced permeability of the sodium channel to calcium without significant changes in the kinetics or the tetrodotoxin sensitivity of the channel. Thus, ANP may regulate the sodium channel by altering its cationic selectivity site to calcium, thereby repressing the sodium current. The suppression of sodium and calcium channels and the resultant depressed excitability of the atrial cells may help to regulate ANP secretion.
authors.affiliation: Department of Physiology, University of Pennsylvania, Philadelphia 19104-6085.
authors.forename: L A
authors.initials: LA
authors.lastname: Sorbera
authors.forename: M
authors.initials: M
authors.lastname: Morad
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism*; D004553:Electric Conductivity; D006168:Guinea Pigs; D006352:Heart Ventricles; D007700:Kinetics; D009206:Myocardium / Q000378:metabolism*; D010539:Permeability; D051381:Rats; D015222:Sodium Channels / Q000187:drug effects / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D015220:Calcium Channels; D015222:Sodium Channels; D013779:Tetrodotoxin; D009320:Atrial Natriuretic Factor; D002118:Calcium