Does stimulation of NaCl secretion in in vitro perfused rectal gland tubules of Squalus acanthias increase membrane capacitance?

1998 ◽  
Vol 436 (4) ◽  
pp. 538-544 ◽  
Author(s):  
R. Greger ◽  
I. Thiele ◽  
R. Warth ◽  
M. Bleich
Keyword(s):  
Membrane Capacitance ◽  
Squalus Acanthias ◽  
Rectal Gland ◽  
Nacl Secretion ◽  
Stimulation Of

Atriopeptin stimulation of rectal gland function in Squalus acanthias

1985 ◽  
Vol 249 (3) ◽  
pp. R348-R354 ◽  
Author(s):  
R. Solomon ◽  
M. Taylor ◽  
D. Dorsey ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Volume Expansion ◽  
Epithelial Transport ◽  
Extracellular Volume ◽  
Chloride Secretion ◽  
Hormonal Control ◽  
Rectal Gland ◽  
Gland Function ◽  
Stimulation Of

The rectal gland of the shark plays a significant role in the homeostasis of extracellular volume. Regulation of rectal gland function is under hormonal control, but the precise identity of the humoral mediator is unknown. Atriopeptin stimulates rectal gland chloride secretion in vivo. This stimulation of epithelial transport is accompanied by systemic and local hemodynamic effects. Atriopeptin also stimulates chloride secretion by the in vitro perfused rectal gland, an effect that is not accompanied by hemodynamic changes. Extracts of shark heart, but not muscle, brain, kidney, or intestine, contain a heat-stable trypsin-sensitive substance capable of in vitro stimulation of rectal gland chloride secretion. Electron micrographic analysis reveals multiple neurosecretory-like granules in atrial cardiocytes that are only rarely seen in ventricular cardiocytes. By using the in vitro perfused gland as a biologic assay, serum obtained after extracellular volume expansion reveals the presence of a rectal gland stimulatory factor that is not present in serum before expansion. These results are consistent with the hypothesis that atriopeptin is present in shark cardiocytes and is released during volume expansion. The atriopeptin stimulates rectal gland chloride secretion, providing a negative feedback mechanism for the regulation of extracellular volume.

Mechanism of active chloride secretion by shark rectal gland: role of Na-K-ATPase in chloride transport

1977 ◽  
Vol 233 (4) ◽  
pp. F298-F306 ◽  
Author(s):  
P. Silva ◽  
J. Stoff ◽  
M. Field ◽  
L. Fine ◽  
J. N. Forrest ◽  
...  
Keyword(s):  
Chloride Transport ◽  
Sodium Concentration ◽  
Chloride Secretion ◽  
Squalus Acanthias ◽  
Rectal Gland ◽  
Tentative Hypothesis ◽  
Shark Rectal Gland ◽  
Electrochemical Equilibrium

The isolated rectal gland of Squalus acanthias was stimulated to secrete chloride against an electrical and a chemical gradient when perfused in vitro by theophylline and/or dibutyryl cyclic AMP. Chloride secretion was depressed by ouabain which inhibits Na-K-ATPase. Thiocyanate and furosemide also inhibited chloride secretion but ethoxzolamide, a carbonic anhydrase inhibitor, did not. Chloride transport was highly dependent on sodium concentration in the perfusate. The intracellular concentration of chloride averaged 70-80 meq/liter in intact glands, exceeding the level expected at electrochemical equilibrium and suggesting active transport of chloride into the cell. These features suggest a tentative hypothesis for chloride secretion by the rectal gland in which the uphill transport of chloride into the cytoplasm is coupled through a membrane carrier to the downhill movement of sodium along its electrochemical gradient. The latter is maintained by the Na-K-ATPase pump while chloride is extruded into the duct by electrical forces.

Mode of activation of salt secretion by C-type natriuretic peptide in the shark rectal gland

1999 ◽  
Vol 277 (6) ◽  
pp. R1725-R1732 ◽  
Author(s):  
Patricio Silva ◽  
Richard J. Solomon ◽  
Franklin H. Epstein
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Chloride Secretion ◽  
Squalus Acanthias ◽  
Rectal Gland ◽  
Stimulatory Action ◽  
Kinase C ◽  
Shark Rectal Gland ◽  
Pkc Activation ◽  
Stimulation Of

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.

Mode of action of somatostatin to inhibit secretion by shark rectal gland

1985 ◽  
Vol 249 (3) ◽  
pp. R329-R334 ◽  
Author(s):  
P. Silva ◽  
J. S. Stoff ◽  
D. R. Leone ◽  
F. H. Epstein
Keyword(s):  
Cellular Response ◽  
Specific Binding ◽  
Phosphodiesterase Inhibitor ◽  
Inhibitory Effect ◽  
Squalus Acanthias ◽  
Rectal Gland ◽  
Gland Cells ◽  
Mechanism Of Inhibition ◽  
Rectal Glands ◽  
Stimulation Of

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.

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