AJP - Renal Physiology, Vol 249, Issue 5 713-F722, Copyright © 1985 by American Physiological Society
cAMP- and beta-adrenergic-stimulated chloride-dependent Ca2+ secretion in frog skin
F. N. Ziyadeh, E. Kelepouris, M. M. Civan and Z. S. Agus
This study examined the possible existence and nature of Ca2+ transport in
frog skin using 45Ca fluxes and short-circuiting technique. Following the
addition to full-thickness frog skin (FTFS) of 8-[p-chlorophenylthio]cAMP
(8-CPT-cAMP), forskolin, or 1-methyl-3-isobutylxanthine, the secretory Ca2+
flux increased severalfold, inducing net Ca2+ secretion. The absorptive
flux was unchanged. Isoproterenol (10(-6)M) reproduced the effects of cAMP
on Ca2+ secretion (-3.76 +/- 0.80 nmol X cm-2 X h-1 vs. +0.04 +/- 0.05 in
control) while vasopressin and parathyroid hormone did not alter Ca2+
fluxes. Because FTFS contains subepidermal glands capable of Cl- secretion
in response to beta-adrenergic stimulation, split-thickness frog skin
(STFS) consisting of the gland-free Na-absorbing surface epithelium was
used to localize the anatomic site of Ca2+ secretion. In STFS, addition of
8-CPT-cAMP or isoproterenol failed to induce Ca2+ secretion, suggesting
that this transport in FTFS is localized in skin glands. Additional studies
explored the relationship between Ca2+ and Cl- transport in FTFS.
Furosemide prevented the stimulation of both Ca2+ and Cl- secretion.
Removal of Cl- from the bathing medium abolished Ca2+ secretion. Thus, FTFS
exhibits a beta-adrenergic, cAMP-stimulated net Ca2+ secretion that is Cl-
dependent. As this effect is not observed in STFS, the pathway of Ca2+
secretion in frog skin is probably localized in the subepidermal glandular
epithelium in association with Cl- secretion. Frog skin glands may
represent a useful model for the study of Ca2+ transport in
Cl--transporting epithelia.
