Bullfrog tadpoles respond to apical application of 100 muM amiloride, acety
lcholine (ACh) or ATP with a sharp transient inward (apical to basolateral)
cation current. In adult. skin, amiloride blockable transepithelial Na+ tr
ansport is upregulated by the hormone aldosterone. Tadpoles were treated in
vivo with aldosterone and changes in short circuit current (Isc) in respon
se to apical application of ATP were determined. Bullfrog tadpoles were exp
osed 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 trea
ted with vehicle alone. Sodium replacement with a large, nonpermeable catio
n resulted in no measurable increase in Isc after exposure to ligand, consi
stent with ATP activation of an inward cation current and not chloride effl
ux. Activation/desensitization time courses and treatment with blockers rev
ealed 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 o
f mRNA associated with P2X channels. Given these data, our working hypothes
is is that all three ligands activate the same process that exhibits both p
urinergic and cholinergic characteristics. These data are consistent with a
ldosterone upregulation of ATP gated channels expressed in the apical membr
ane of larval frog skin.