Eur J Pharmacol 1994 May 17;2673:281-7. doi: 10.1016/0922-4106(94)90152-x.

Atrial natriuretic factor potentiates glibenclamide-sensitive K+ currents via the activation of receptor guanylate cyclase in follicle-enclosed Xenopus oocytes.

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The effect of the atrial natriuretic factor (ANF) on K+ channel opener-induced glibenclamide-sensitive K+ currents was studied using follicle-enclosed Xenopus oocytes. K+ currents induced by the K+ channel opener Y-26763 were potentiated by ANF (0.5-50 nM) in a concentration-dependent 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 cGMP contents of follicle-enclosed oocytes; about 13-fold increase was achieved by 100 nM ANF, showing a peak at 5 min. The ANF-stimulated accumulation of cGMP was suppressed by HS-142-1 (a non-peptide antagonist of the ANF receptor), at concentrations of 3-300 micrograms/ml. The K+ current-potentiating effect of ANF was mimicked by membrane-permeable cGMP (1 mM 8-bromo cGMP). These results suggest that ANF potentiates glibenclamide-sensitive K+ currents via the activation of receptor guanylate cyclase and consequent accumulation of cGMP in follicle-enclosed Xenopus oocytes.

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Species referenced: Xenopus laevis
Genes referenced: nppa