Ion Secretion and Isotonic Transport in Frog Skin Glands

1996 ◽  
Vol 152 (2) ◽  
pp. 101-110 ◽  
Author(s):  
H.H. Ussing ◽  
F. Lind ◽  
E.H. Larsen
Keyword(s):  
Frog Skin ◽  
Skin Glands ◽  
Ion Secretion ◽  
Frog Skin Glands

Chloride transport in glands of frog skin

1983 ◽  
Vol 244 (3) ◽  
pp. C221-C226 ◽  
Author(s):  
I. G. Thompson ◽  
J. W. Mills
Keyword(s):  
Frog Skin ◽  
Chloride Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Serosal Side ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Skin Glands ◽  
Frog Skin Glands ◽  
Beta Adrenergic Agonist

The effects of beta-adrenergic stimulation on the bidirectional fluxes of Na+ and Cl- across the frog skin glands were determined. Isoproterenol elicited net serosal-to-mucosal fluxes of both Na+ (JNanet) and Cl- (JClnet) equal to 0.19 +/- 0.05 (SE) and 0.57 +/- 0.05 mueq X cm-2 X h-1, respectively. The residual current (JClnet - JNanet) of 0.38 +/- 0.05 mueq X cm-2 X h-1 closely approximates the isoproterenol-induced short-circuit current of 0.30 +/- 0.04 mueq X cm-2 X h-1. Furosemide added to the serosal side prior to isoproterenol inhibited the isoproterenol-induced net fluxes of both Na+ and Cl-. The addition of dibutyryl cAMP and 3-isobutyl-1-methylxanthine to the serosal side mimicked the action of isoproterenol by stimulating glandular short-circuit current. We conclude that an active Cl(-)-transport mechanism resides in the frog skin glands and is 1) stimulated by a beta-adrenergic agonist (its action is mimicked by cAMP) and 2) inhibited by the loop diuretic furosemide.

scholarly journals Nerve Stimulation and Electrical Properties of Frog Skin

1969 ◽  
Vol 53 (4) ◽  
pp. 427-449 ◽  
Author(s):  
Barry D. Lindley
Keyword(s):  
Electrical Properties ◽  
Electromotive Force ◽  
Frog Skin ◽  
Short Circuit ◽  
Ionic Composition ◽  
Short Circuit Current ◽  
Exocrine Glands ◽  
Skin Glands ◽  
Chord Conductance ◽  
Frog Skin Glands

The suitability of frog skin glands as a model for the study of secretory mechanisms in exocrine glands was explored. Periodic voltage clamp was used to determine continually the short-circuit current, chord conductance, and electromotive force of frog skin during neural and pharmacological activation of the skin glands. Both the chord conductance and the short-circuit current increased with glandular activation; the temporal dissociation of these increases suggests that there are at least two separate components to the secretory response. The sensitivity of the secretory electrical changes to changes in the ionic composition of the bathing solutions supports the notion of electrogenic chloride active transport as being basic to the activity of the exocrine glands.

On the Histology of Frog Skin Glands

1944 ◽  
Vol 63 (3) ◽  
pp. 254 ◽  
Author(s):  
Glenn A. Noble ◽  
Elmer R. Noble
Keyword(s):  
Frog Skin ◽  
Skin Glands ◽  
Frog Skin Glands

Relationships between calcium and chloride transport in frog skin glands

1986 ◽  
Vol 251 (4) ◽  
pp. F647-F654 ◽  
Author(s):  
F. N. Ziyadeh ◽  
E. Kelepouris ◽  
Z. S. Agus
Keyword(s):  
Frog Skin ◽  
Chloride Transport ◽  
Short Circuit ◽  
Calcium Ionophore ◽  
Ionophore A23187 ◽  
Bathing Medium ◽  
Beta Adrenergic ◽  
Cl Secretion ◽  
Skin Glands ◽  
Frog Skin Glands

Frog skin gland, a furosemide-sensitive Cl(-)-secreting epithelium, exhibits Cl(-)-dependent Ca2+ secretion in response to stimulation by beta-adrenergic agonists. In this study, we further explored the relationships between Cl- and Ca2+ secretion in frog skin using 45Ca fluxes and short-circulating technique. On addition of isoproterenol (ISO) or 8-(p-chlorophenylthio)-cAMP, a significant positive correlation was demonstrated between Ca2+ secretion and Cl- secretion. Because Cl- transport in other Cl(-)-transporting epithelia may be modulated by prostaglandins or by changes in cytosolic Ca2+ activity, in addition to modulation by cAMP, we also examined the effects of prostaglandins (PG)E2 and F2 alpha, indomethacin (INDO), and the calcium ionophore A23187. Treatment with PGE2, PGF2 alpha, or A23187 at a dose of 10(-5) M resulted in marked stimulation in the amiloride-resistant short-circuit current, a reflection of Cl- secretion. This current was inhibited by furosemide addition or removal of Cl- from the bathing medium. However, and in contrast to stimulation with ISO or cAMP, PGE2, PGF2 alpha, and A23187 failed to induce Ca2+ secretion. In addition, the stimulation of Cl- secretion by A23187 was abolished by INDO (10(-6) M) pretreatment. Thus frog skin glands secrete Cl- via two mechanisms: one mediated by beta-adrenergic-cAMP stimulation and the other by activation of prostaglandin metabolism induced by changes in cytosolic Ca2+. Only the former pathway is associated with Ca2+ secretion. Furthermore, to account for the Cl- dependence of Ca2+ secretion, we postulate the existence of a Ca2+-Cl- cotransport system stimulated by cAMP.

cAMP- and beta-adrenergic-stimulated chloride-dependent Ca2+ secretion in frog skin

1985 ◽  
Vol 249 (5) ◽  
pp. F713-F722 ◽  
Author(s):  
F. N. Ziyadeh ◽  
E. Kelepouris ◽  
M. M. Civan ◽  
Z. S. Agus
Keyword(s):  
Frog Skin ◽  
Surface Epithelium ◽  
Adrenergic Stimulation ◽  
Anatomic Site ◽  
Bathing Medium ◽  
Beta Adrenergic ◽  
Cl Secretion ◽  
Skin Glands ◽  
Frog Skin Glands ◽  
Absorptive Flux

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.

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