Cyclic AMP regulation of active chloride transport in the rectal gland of marine elasmobranchs

1977 ◽  
Vol 199 (3) ◽  
pp. 443-448 ◽  
Author(s):  
Jeffrey S. Stoff ◽  
Patricio Silva ◽  
Michael Field ◽  
John Forrest ◽  
Arthur Stevens ◽  
...  
1994 ◽  
Vol 196 (1) ◽  
pp. 405-418 ◽  
Author(s):  
J R Riordan ◽  
B Forbush ◽  
J W Hanrahan

Transepithelial Cl- secretion in vertebrates is accomplished by a secondary active transport process brought about by the coordinated activity of apical and basolateral transport proteins. The principal basolateral components are the Na+/K(+)-ATPase pump, the Na+/K+/2Cl- cotransporter (symporter) and a K+ channel. The rate-limiting apical component is a cyclic-AMP-stimulated Cl- channel. As postulated nearly two decades ago, the net Cl- movement from the blood to the lumen involves entry into the epithelial cells with Na+ and K+, followed by active Na+ extrusion via the pump and passive K+ exit via a channel. Intracellular [Cl-] is raised above electrochemical equilibrium and exits into the lumen when the apical Cl- channel opens. Cl- secretion is accompanied by a passive paracellular flow of Na+. The tubules of the rectal glands of elasmobranchs are highly specialized for secreting concentrated NaCl by this mechanism and hence have served as an excellent experimental model in which to characterize the individual steps by electrophysiological and ion flux measurements. The recent molecular cloning and heterologous expression of the apical Cl- channel and basolateral cotransporter have enabled more detailed analyses of the mechanisms and their regulation. Not surprisingly, since hormones acting through kinases control secretion, both the Cl- channel, which is the shark counterpart of the CFTR (Cystic Fibrosis Transmembrane Conductance Regulator), and the cotransporter are regulated by phosphorylation and dephosphorylation. The primary stimulation of secretion by hormones employing cyclic AMP as second messenger activates CFTR via the direct action of protein kinase A (PKA), which phosphorylates multiple sites on the R domain. In contrast, phosphorylation of the cotransporter by as yet unidentified kinases is apparently secondary to the decrease in intracellular chloride concentration caused by anion exit through CFTR.


1979 ◽  
Vol 237 (2) ◽  
pp. F138-F144 ◽  
Author(s):  
J. S. Stoff ◽  
R. Rosa ◽  
R. Hallac ◽  
P. Silva ◽  
F. H. Epstein

Active transport of chloride is modulated by cyclic AMP in the rectal gland of Squalus acanthias. Vasoactive intestinal peptide (VIP) specifically activates the production of cyclic AMP by the gland and stimulates the secretion of chloride. Somatostatin inhibits VIP-induced secretion but has no effect alone. Both these peptides are present in the dogfish shark and may play an important role in electrolyte homeostasis.


1984 ◽  
Vol 154 (2) ◽  
pp. 139-144 ◽  
Author(s):  
Patricio Silva ◽  
Kate Spokes ◽  
Jonathan A. Epstein ◽  
Arthur Stevens ◽  
Franklin H. Epstein

1989 ◽  
Vol 36 (5) ◽  
pp. 760-767 ◽  
Author(s):  
Yasuhiro Ando ◽  
Kaoru Tabei ◽  
Hiroaki Furuya ◽  
Yasushi Asano

1980 ◽  
Vol 53 (3) ◽  
pp. 215-221 ◽  
Author(s):  
Patricio Silva ◽  
Jeffrey S. Stoff ◽  
Richard J. Solomon ◽  
Robert Rosa ◽  
Arthur Stevens ◽  
...  

1975 ◽  
Vol 228 (6) ◽  
pp. 1808-1814 ◽  
Author(s):  
HN Nellans ◽  
RA Frizzell ◽  
SG Schultz

Acetazolamide (8 mM) aboishes active Cl absorption and inhibits but does not abolish active Na absorption by stripped, short-circuited rabbit ileum. These effects are not accompanied by significant changes in the transmural electrical potential difference or short-circuit current. Studies of the undirectional influxes of Na andCl indicate that acetazolamide inhibits the neutral, coupled NaCl influx process at the mucosal membranes. This action appears to explain the observed effect of acetazolamide on active, transepithelial Na and Cl transport. Acetazolamide did not significantly inhibit either spontaneous or theophylline-induced Cl secretion by this preparation, suggesting that the theophylline-induced secretion may not simply be due tothe unmasking of a preexisting efflux process when the neutral influx mechanism is inhibited by theophylline. Finally, inhibition of the neutral NaCl influx process by acetazolamide does not appear to be attributable to an inhibition of endogenous HCO3production or an elevation in intracellular cyclic-AMP levels. Instead, it appearstheat the effect of acetazolamide is due to a direct interaction with a membrane component involved in the coupled influx process.


1986 ◽  
Vol 94 (3) ◽  
pp. 205-215 ◽  
Author(s):  
D. Marver ◽  
S. Lear ◽  
L. T. Marver ◽  
P. Silva ◽  
F. H. Epstein

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