Atrionatriuretic peptide suppressed calcium and sodium currents in rat and guinea pig ventricular myocytes by enhancing the permeability of the sodium channel to calcium.
ANP suppresses sodium and calcium currents in ventricular myocytes by altering the cationic selectivity site of the sodium channel to calcium, which may help regulate ANP secretion.
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.
Sorbera et al. (Fri,) reported a other. Atrionatriuretic peptide (ANP) was evaluated on Calcium and sodium currents. Atrionatriuretic peptide suppressed calcium and sodium currents in rat and guinea pig ventricular myocytes by enhancing the permeability of the sodium channel to calcium.