The absence of any effect of alpha-human atrial natriuretic peptide on sodium transport and osmotic water flow in the toad bladder.
Synthesized alpha-human atrial natriuretic peptide (alpha-hANP), at 10(-6) M, failed to inhibit short-circuit current and basal and 10 mU/ml vasopressin-stimulated osmotic water flow in the bladder either pretreated with cyclooxygenase inhibitor, or preincubated with arachidonic acid, a precursor of PGE2. These results indicate alpha-hANP to have no direct effect on sodium transport and water permeability in the bladder, and no evidence was obtained indicating that alpha-hANP suppresses vasopressin-stimulated water flow by increasing PGE2 production.
D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D001692:Biological Transport / Q000187:drug effects; D002023:Bufo bufo; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*; D001743:Urinary Bladder / Q000378:metabolism*; D014667:Vasopressins / Q000494:pharmacology; D014882:Water-Electrolyte Balance / Q000187:drug effects*
D001095:Arachidonic Acids; D014667:Vasopressins; D009320:Atrial Natriuretic Factor; D012964:Sodium; D007213:Indomethacin