Stimulation of NaCl secretion in the rectal gland of the dogfish Squalus acanthias

1988 ◽  
Vol 90 (4) ◽  
pp. 733-737 ◽  
Author(s):  
R Greger ◽  
H Gögeleinf ◽  
E Schlatter
1999 ◽  
Vol 277 (6) ◽  
pp. R1725-R1732 ◽  
Author(s):  
Patricio Silva ◽  
Richard J. Solomon ◽  
Franklin H. Epstein

We studied the modes of activation of the salt-secreting rectal gland of the spiny dogfish, Squalus acanthias, by the native cardiac peptide CNP. The stimulatory action of CNP in isolated perfused glands is inhibited by 10 mM procaine, presumably by blocking release of vasoactive intestinal peptide (VIP) from nerves. Procaine reduces the slope of the dose-response curve of human CNP and that of shark CNP (each P < 0.0001). CNP increases short-circuit current in cultured rectal gland cells from 4.8 ± 1.6 to 27.0 ± 7.8 μA/cm2. It also stimulates the secretion of chloride in isolated perfused glands in the presence of 10 mM procaine from 72 ± 31 to 652 ± 173 μeq ⋅ h−1 ⋅ g−1. These results suggest that CNP has a direct cellular action not mediated by the neural release of VIP. The residual stimulation of perfused glands in the presence of procaine was almost completely inhibited by staurosporine [10 nM; an inhibitor of protein kinase C (PKC)] from 652 ± 173 to 237 ± 61 μeq ⋅ h−1 ⋅ g−1. Although CNP stimulates guanylyl cyclase in shark rectal gland, chloride secretion of perfused glands was not elicited by 8-bromoadenosine-cGMP (8-BrcGMP) alone nor by the activator of PKC phorbol ester. The combination of PKC activation and 8-BrcGMP infusion, however, stimulated chloride secretion in perfused glands from 94 ± 30 to 506 ± 61 μeq ⋅ h−1 ⋅ g−1, a level comparable to that observed in glands blocked with procaine. Several parallel pathways appear to be synergistic in activating chloride secretion stimulated by CNP in the rectal gland.


1985 ◽  
Vol 249 (3) ◽  
pp. R329-R334 ◽  
Author(s):  
P. Silva ◽  
J. S. Stoff ◽  
D. R. Leone ◽  
F. H. Epstein

The rectal gland of the spiny dogfish Squalus acanthias is stimulated to secrete chloride by vasoactive intestinal peptide (VIP) in a way that is inhibited by somatostatin. The mechanism of inhibition by somatostatin was studied in isolated perfused rectal glands and separated rectal gland cells. Somatostatin did not alter the specific binding of VIP to rectal gland cells but inhibited their accumulation of adenosine 3',5'-cyclic monophosphate (cAMP) in response to VIP. In isolated perfused glands, somatostatin inhibited the stimulation of secretion produced by VIP, adenosine, and forskolin, as well as by dibutyryl cAMP plus a phosphodiesterase inhibitor. The results support the hypothesis of both a proximal and a distal locus, in the cascade of events leading from adenylate cyclase activation to cellular response, at which somatostatin exerts an inhibitory effect.


1984 ◽  
Vol 402 (4) ◽  
pp. 376-384 ◽  
Author(s):  
Rainer Greger ◽  
Eberhard Schlatter ◽  
Fong Wang ◽  
John N. Forrest

1992 ◽  
Vol 262 (4) ◽  
pp. R707-R711 ◽  
Author(s):  
R. Solomon ◽  
A. Protter ◽  
G. McEnroe ◽  
J. G. Porter ◽  
P. Silva

Homologous shark C-type natriuretic peptide (sCNP) was infused as a bolus and as a constant infusion in the isolated perfused rectal gland of the same species, Squalus acanthias. sCNP was a potent stimulator of chloride secretion similar in its dose-response curve to vasoactive intestinal peptide. sCNP was equipotent with killifish CNP but more potent than human CNP (hCNP). Truncated and substituted, forms of hCNP were also capable of stimulation of chloride secretion in the order hCNP greater than hCNP (6-22) = [Gly9]hCNP greater than hCNP-(7-21). sCNP was more potent than human atrial natriuretic peptide (hANP), which was more potent than porcine brain natriuretic peptide. hANP-(31-67) was without effect. These studies suggest that sCNP may be the physiological regulator of rectal gland function. The receptor in the rectal gland is unknown but based on the order of potencies, position 4 in the NH2-terminal end and the ring itself are important for ligand effects.


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