scholarly journals Feeding through your gills and turning a toxicant into a resource: how the dogfish shark scavenges ammonia from its environment

2016 ◽  
Vol 219 (20) ◽  
pp. 3218-3226 ◽  
Author(s):  
Chris M. Wood ◽  
Marina Giacomin
Keyword(s):  
1999 ◽  
Vol 202 (24) ◽  
pp. 3605-3610 ◽  
Author(s):  
D.H. Evans ◽  
M.P. Gunderson

Endothelins (ETs) are potent vasoconstrictive peptides that are secreted by the vascular endothelium and other tissues in vertebrates. Previous studies have demonstrated that ETs are expressed in a variety of fish tissues and contract various blood vessels. In order to determine if receptors for ET are expressed in fish gill tissue, we examined the binding kinetics of (125)I-labeled, human ET-1 to membrane fragments isolated from the gill of the dogfish shark, Squalus acanthias. (125)I-ET-1 bound at a single site, with a dissociation constant (K(d)) and binding site number (B(max)) very similar to those described in a variety of mammalian blood vessels. ET-1 and ET-3 competed equally with (125)I-ET-1, suggesting that the receptor was ET(B), which has been shown in mammalian systems to bind to both ligands equally. The ET(B)-specific agonists sarafotoxin S6c, IRL-1620, and BQ-3020 also competed against (125)I-ET-1 at a single site, supporting this hypothesis. We conclude that the shark gill expresses an ET(B) receptor with substantial homology to the mammalian receptor and that ET may play an important role in modulating such vital gill functions as gas exchange, ion regulation, acid-base balance, and excretion of nitrogen.


2006 ◽  
Vol 291 (2) ◽  
pp. R464-R472 ◽  
Author(s):  
Carsten H. Baehr ◽  
Gert Fricker ◽  
David S. Miller

The vertebrate choroid plexus removes potentially toxic metabolites and xenobiotics from cerebrospinal fluid (CSF) to blood for subsequent excretion in urine and bile. We used confocal microscopy and quantitative image analysis to characterize the mechanisms driving transport of the large organic anion, fluorescein-methotrexate (FL-MTX), from bath (CSF-side) to blood vessels in intact lateral choroid plexus from dogfish shark, Squalus acanthias, an evolutionarily ancient vertebrate. With 2 μM FL-MTX in the bath, steady-state fluorescence in the subepithelium/vascular space exceeded bath levels by 5- to 10-fold, and fluorescence in the epithelial cells was slightly below bath levels. FL-MTX accumulation in both tissue compartments was reduced by NaCN, Na removal, and ouabain, but not by a 10-fold increase in medium K. Certain organic anions, e.g., probenecid, MTX, and taurocholate, reduced FL-MTX accumulation in both tissue compartments; p-aminohippurate and estrone sulfate reduced subepithelial/vascular accumulation, but not cellular accumulation. At low concentrations, digoxin, leukotriene C4, and MK-571 reduced fluorescence in the subepithelium/vascular space while increasing cellular fluorescence, indicating preferential inhibition of efflux over uptake. In the presence of 10 μM digoxin (reduced efflux, enhanced cellular accumulation), cellular FL-MTX accumulation was specific, concentrative, and Na dependent. Thus transepithelial FL-MTX transport involved the following two carrier-mediated steps: electroneutral, Na-dependent uptake at the apical membrane and electroneutral efflux at the basolateral membrane. Finally, FL-MTX accumulation in both tissue compartments was reduced by phorbol ester and increased by forskolin, indicating antagonistic modulation by protein kinase C and protein kinase A.


1987 ◽  
Vol 252 (1) ◽  
pp. F99-F103 ◽  
Author(s):  
P. Silva ◽  
J. S. Stoff ◽  
R. J. Solomon ◽  
S. Lear ◽  
D. Kniaz ◽  
...  

Salt secretion by the isolated perfused rectal gland of the spiny dogfish shark, Squalus acanthias, is stimulated by synthetic rat atrial natriuretic peptide (ANP II) as well as extracts of shark heart, but not by 8-bromo-cyclic guanosine 5'-monophosphate. Cardiac peptides have no effect on isolated rectal gland cells or perfused tubules, suggesting that stimulation requires an intact gland. The stimulation of secretion by ANP II is eliminated by maneuvers that block neurotransmitter release. These include: perfusion with procaine (10(-2) M), perfusion with high Mg2+ (9.5 mM) and low Ca2+ (0.5 mM) concentrations, and addition to the perfusate of the calcium channel blockers nifedipine (10(-6)M), diltiazem (5 X 10(-5)M), or verapamil (10(-4)M). Cardiac peptides stimulate the release of vasoactive intestinal peptide (VIP), known to be present in rectal gland nerves, into the venous effluent or perfused glands in parallel with their stimulation of salt secretion, but the release of VIP induced by ANP II is prevented by perfusion with procaine. Cardiac peptides thus appear to regulate rectal gland secretion by releasing VIP from neural stores within the gland. It is possible that other physiological effects of these hormones might be explained by an action to enhance local release of neurotransmitters.


1992 ◽  
Vol 262 (4) ◽  
pp. C1000-C1008 ◽  
Author(s):  
B. Forbush ◽  
M. Haas ◽  
C. Lytle

To investigate regulation of the Na-K-Cl cotransport system in the rectal gland of the dogfish shark Squalus acanthias, we examined binding of the loop diuretic [3H]benzmetanide to the intact gland. Glands were perfused with a shark Ringer solution, either in a basal state or stimulated with vasoactive intestinal peptide (VIP). [3H]benzmetanide was added to the perfusion solution for the last 25 min of perfusion, after which the gland was homogenized and the amount of bound [3H]benzmetanide was determined in the membrane fraction. Most of the membrane-associated [3H]-benzmetanide appeared to be associated with the Na-K-Cl cotransporter as judged by the dissociation rates at 0 degree C and 20 degrees C, by labeling with a photosensitive analogue, and by continued association of [3H]benzmetanide with membrane protein on solubilization. With the use of [3H]4-benzoyl-5-sulfamoyl-3-(3- thenyloxy)benzoic acid, a photosensitive analogue of benzmetanide, a 200-kDa protein was selectively labeled on exposure to ultraviolet light. It was also possible to detect [3H]-benzmetanide binding during the perfusion period as an arterial-venous difference, thereby providing a time course of the binding process. In comparing two groups of five glands each, VIP stimulated NaCl secretion 20-fold and [3H]benzmetanide binding 16-fold, providing strong evidence that the Na-K-Cl cotransport system is activated as part of the process of stimulation of secretion. The VIP-stimulated increase in [3H]benzmetanide binding was completely inhibited when Ba was added to the perfusate to block K channel-mediated K exit across the basolateral membrane.(ABSTRACT TRUNCATED AT 250 WORDS)


2007 ◽  
Vol 156 (2) ◽  
pp. 220-228 ◽  
Author(s):  
Chris M. Wood ◽  
R. Stephen Munger ◽  
Jill Thompson ◽  
Trevor J. Shuttleworth

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