title: Aldosterone upregulates purinergic responses in larval amphibian skin epithelium.
abstract: Bullfrog tadpoles respond to apical application of 100 microM amiloride, acetylcholine (ACh) or ATP with a sharp transient inward (apical to basolateral) cation current. In adult skin, amiloride blockable transepithelial Na+ transport is upregulated by the hormone aldosterone. Tadpoles were treated in vivo with aldosterone and changes in short circuit current (Isc) in response to apical application of ATP were determined. Bullfrog tadpoles were exposed to aldosterone (10(-6) M) for periods ranging from 3 h to 60 h. Skins from 60-h aldosterone-treated animals showed a two- to three-fold increase in apical ATP-activated short circuit current when compared to animals treated with vehicle alone. Sodium replacement with a large, nonpermeable cation resulted in no measurable increase in Isc after exposure to ligand, consistent with ATP activation of an inward cation current and not chloride efflux. Activation/desensitization time courses and treatment with blockers revealed no measurable differences between aldosterone-treated and non-treated skins. Activation by amiloride and ACh gave essentially identical results. Studies with RT/PCR showed significant increases over controls of levels of mRNA associated with P2X channels. Given these data, our working hypothesis is that all three ligands activate the same process that exhibits both purinergic and cholinergic characteristics. These data are consistent with aldosterone upregulation of ATP gated channels expressed in the apical membrane of larval frog skin.
authors.affiliation: Department of Physiology, Southern Illinois University, Carbondale 62901, USA.
authors.forename: D
authors.initials: D
authors.lastname: Holbird
authors.forename: P
authors.initials: P
authors.lastname: Jensik
authors.forename: T
authors.initials: T
authors.lastname: Cox
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000378:metabolism; D000450:Aldosterone / Q000494:pharmacology*; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D004232:Diuretics / Q000494:pharmacology; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism*; D015870:Gene Expression / Q000502:physiology; D007814:Larva / Q000502:physiology; D018727:Muscarinic Antagonists / Q000494:pharmacology; D018733:Nicotinic Antagonists / Q000494:pharmacology; D011188:Potassium / Q000493:pharmacokinetics; D058919:Purinergic P2 Receptor Antagonists; D012333:RNA, Messenger / Q000032:analysis; D011892:Rana catesbeiana / Q000254:growth & development*; D018048:Receptors, Purinergic P2 / Q000235:genetics / Q000378:metabolism*; D058848:Receptors, Purinergic P2X4; D058485:Receptors, Purinergic P2X5; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012867:Skin / Q000166:cytology*; D012964:Sodium / Q000493:pharmacokinetics; D013449:Sulfonamides / Q000494:pharmacology; D013498:Suramin / Q000494:pharmacology; D014403:Tubocurarine / Q000494:pharmacology; D015854:Up-Regulation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000970:Antineoplastic Agents; D004232:Diuretics; D018727:Muscarinic Antagonists; D018733:Nicotinic Antagonists; D058919:Purinergic P2 Receptor Antagonists; D012333:RNA, Messenger; D018048:Receptors, Purinergic P2; D058848:Receptors, Purinergic P2X4; D058485:Receptors, Purinergic P2X5; D013449:Sulfonamides; D014665:Vasodilator Agents; D000450:Aldosterone; D013498:Suramin; C017967:W 7; D001285:Atropine; D000584:Amiloride; D000255:Adenosine Triphosphate; D012964:Sodium; D000109:Acetylcholine; D011188:Potassium; D014403:Tubocurarine