ATRIAL-NATRIURETIC-FACTOR POTENTIATES GLIBENCLAMIDE-SENSITIVE K-CYCLASE IN FOLLICLE-ENCLOSED XENOPUS-OOCYTES( CURRENTS VIA THE ACTIVATION OF RECEPTOR GUANYLATE)

The effect of the atrial natriuretic factor (ANF) on K+ channel opener -induced glibenclamide-sensitive K+ currents was studied using follicl e-enclosed Xenopus oocytes. K+ currents induced by the K+ channel open er Y-26763 were potentiated by ANF (0.5-50 nM) in a concentration-depe ndent manner. 50 nM ANF increased the peak amplitude of the current by 59.4 +/- 9.9% (mean +/- S.E., n = 8). ANF (1-1000 nM) increased the c GMP contents of follicle-enclosed oocytes; about 13-fold increase was achieved by 100 nM ANF, showing a peak at 5 min. The ANF-stimulated ac cumulation of cGMP was suppressed by HS-142-1 (a non-peptide antagonis t of the ANF receptor), at concentrations of 3-300 mu g/ml. The K+ cur rent-potentiating effect of ANF was mimicked by membrane-permeable cGM P (1 mM 8-bromo cGMP). These results suggest that ANF potentiates glib enclamide-sensitive K+ currents via the activation of receptor guanyla te cyclase and consequent accumulation of cGMP in follicle-enclosed Xe nopus oocytes.