Comparative study of cardiac electrophysiological effects of atrial natriuretic peptide

The effects of atrial natriuretic peptide (ANP) on action potential characteristics were studied in various (human, rabbit, guineapig) atrial and guinea-pig right ventricular papillary muscles. ANP (1-100 nM) did not modify the resting membrane potential nor the maximum rate of depolarization phase (V-max). Up to 10 nM, ANP dose-dependently decreased the action potential amplitude both in guinea-pig atrial and ventricular muscles, but it did not affect this parameter in the other atrial preparations. ANP caused a dose-dependent, marked decrease of action potential duration (APD) in practically every cardiac preparation studied (exception of guinea-pig left atrium). The strongest effect on APD can be observed in human atrial and guinea-pig ventricular fibers. The K+ channel blocker 4-aminopyridine (1 mM) and the ATP-dependent K+ channel inhibitor glibenclamide (10 mu M) prevented the effect of ANP on APD in both ventricular atrial preparations. ANP prevented the appearance of isoprenaline (0.5 mu M) induced slow AP in K+ depolarized myocardium. The present data suggest that ANP may inhibit the slow inward Ca2+ channel activity and facilitate the K+ channel activity.