C-type natriuretic peptides stimulate chloride secretion in the rectal gland of Squalus acanthias

1992 ◽  
Vol 262 (4) ◽  
pp. R707-R711 ◽  
Author(s):  
R. Solomon ◽  
A. Protter ◽  
G. McEnroe ◽  
J. G. Porter ◽  
P. Silva
Keyword(s):  
Natriuretic Peptide ◽  
Response Curve ◽  
Chloride Secretion ◽  
Squalus Acanthias ◽  
Constant Infusion ◽  
Rectal Gland ◽  
Ligand Effects ◽  
Physiological Regulator ◽  
Gland Function ◽  
Stimulation Of

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.

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.

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.

In vivo effect of volume expansion on rectal gland function. I. Humoral factors

1984 ◽  
Vol 246 (1) ◽  
pp. R63-R66 ◽  
Author(s):  
R. Solomon ◽  
M. Taylor ◽  
J. S. Stoff ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Volume Expansion ◽  
Chloride Secretion ◽  
Ringer Solution ◽  
Squalus Acanthias ◽  
Humoral Factor ◽  
Rectal Gland ◽  
Host Fish ◽  
Humoral Factors ◽  
Gland Function

The spiny dogfish Squalus acanthias responds to volume expansion by increasing the rate of chloride secretion by its rectal gland. The response is elicited by intravascular infusion of either isotonic shark Ringer solution, a 1 M hypertonic sodium chloride solution, or an isotonic hyponatremic solution containing equal volumes of shark Ringer solution and 10% mannitol. The effect of volume expansion was evoked in explanted glands connected to a host fish only by the arterial supply, indicating that the response is mediated by a humoral factor. The explanted gland responded to theophylline (2.5 X 10(-3) M) and adenosine 3',5'-cyclic monophosphate (5 X 10(-4) M) by increasing the rate of secretion of chloride by an amount similar to that induced by volume expansion of the perfusing fish. Theophylline at concentrations (10(-6) to 5 X 10(-5) M) that are known to inhibit the effect of adenosine in isolated perfused glands failed to inhibit the effect of volume expansion on explanted glands. Somatostatin (4.5 X 10(-6) M), which inhibits the effect of vasoactive intestinal peptide (VIP) in the isolated perfused gland, completely prevented the secretory response to volume expansion in explanted glands. Volume expansion is a major stimulus for chloride secretion by the rectal gland. The effect is mediated by a humoral factor that appears to be VIP.

Primary role of volume expansion in stimulation of rectal gland function

1985 ◽  
Vol 248 (5) ◽  
pp. R638-R640 ◽  
Author(s):  
R. Solomon ◽  
M. Taylor ◽  
S. Sheth ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Plasma Volume ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Chloride Secretion ◽  
Ringer Solution ◽  
Rectal Gland ◽  
Primary Role ◽  
Fourfold Increase ◽  
Gland Function

Chloride secretion by the in vivo rectal gland of the shark is stimulated by the intravascular infusion of salt solutions of varying osmolar and sodium concentration. In a cross-perfused and denervated rectal gland, the infusion of a small amount of a hypertonic salt solution raises plasma osmolality but does not increase plasma volume in the donor fish. Under these conditions, rectal gland chloride secretion is not stimulated. A subsequent infusion of isotonic shark Ringer solution increases plasma volume 50%, decreases plasma osmolality, and produces a fourfold increase in chloride secretion and a threefold decrease in vascular resistance within the gland. Both the vasodilatory and secretory responses also follow the infusion of a hypotonic shark Ringer solution. The data further support the hypothesis that the rectal gland of the shark is involved in the regulation of intravascular volume rather than in osmoregulation.

Neural control of shark rectal gland

1988 ◽  
Vol 255 (2) ◽  
pp. R212-R216 ◽  
Author(s):  
J. S. Stoff ◽  
P. Silva ◽  
R. Lechan ◽  
R. Solomon ◽  
F. H. Epstein
Keyword(s):  
Neural Control ◽  
Squalus Acanthias ◽  
Rectal Gland ◽  
Channel Blockers ◽  
Stimulatory Action ◽  
Histological Techniques ◽  
Neuronal Tissue ◽  
Neural Modulation ◽  
Veratrum Alkaloids ◽  
Gland Function

Veratrum alkaloids stimulated salt secretion by the isolated perfused rectal gland of Squalus acanthias. Stimulation by veratrine was prevented by the nerve channel blockers tetrodotoxin and procaine and was not evident in a preparation of dispersed rectal gland cells. Vasoactive intestinal peptide (VIP)-like immunoreactivity was detected by histological techniques in neuronal tissue within the rectal gland. Veratrine stimulation caused the release of immunoreactive VIP into the venous effluent of perfused glands. The stimulatory action of veratrine was inhibited by somatostatin, another neuropeptide known to be present in nerves of Squalus rectal gland. These findings suggest the likelihood of neural modulation of rectal gland function.

Sodium Chloride Secretion in Rectal Gland of Dogfish, Squalus acanthias

Physiology ◽  
1986 ◽  
Vol 1 (4) ◽  
pp. 134-136
Author(s):  
R. Greger ◽  
E. Schlatter ◽  
H. Gögelein
Keyword(s):  
Sodium Chloride ◽  
Basic Principle ◽  
Peptide Hormones ◽  
Chloride Secretion ◽  
Hormonal Control ◽  
Squalus Acanthias ◽  
Rectal Gland

The rectal gland of the dogfish is specialized for the secretion of sodium chloride. The secretion is controlled by peptide hormones such as, for example, vasointestinal peptide. The mechanism of sodium chloride secretion is apparently similar to that present in mammalian epithelia such as the colon and trachea. This essay discusses the basic principle of sodium chloride secretion in the rectal gland and the mechanism of its hormonal control.

C-type natriuretic peptide receptors and signaling in rectal gland of Squalus acanthias

1993 ◽  
Vol 264 (2) ◽  
pp. F300-F305 ◽  
Author(s):  
M. Gunning ◽  
C. Cuero ◽  
R. Solomon ◽  
P. Silva
Keyword(s):  
Natriuretic Peptide ◽  
Guanylate Cyclase ◽  
Plasma Membranes ◽  
Chloride Secretion ◽  
Ring Structure ◽  
Significant Loss ◽  
Rectal Gland ◽  
Peptide Receptors ◽  
Natriuretic Peptide Receptors ◽  
Similar Affinity

Recent evidence suggests that the newly described natriuretic peptide, C-type natriuretic peptide (CNP), may be the circulating form of natriuretic peptide in the shark. In the shark CNP has a major site of action in the rectal gland, which augments chloride secretion in response to stimulation by volume loading or CNP infusion. We therefore examined the shark rectal gland for natriuretic peptide receptors and determined the presence of guanylate cyclase-linked receptors and non-guanylate cyclase-linked receptors for CNP in this tissue. CNP binds with uniform high affinity (dissociation constant of 78 +/- 11 pM) to receptors of high density (receptor density of 61 +/- 0.7 fmol/mg protein) in plasma membranes prepared from the rectal gland. By use of rat atrial natriuretic peptide (rANP) as a competing ligand, two classes of receptors become apparent in this population, both of which have similar affinity for CNP, but different affinities for rANP. The low-molecular-weight natriuretic peptide receptor-specific peptide, des-[Gln116,Ser117,Gly118, Leu119,Gly120]rANP-(102-121), binds to 50% of the receptors in the rectal gland, but fails to bind to the remaining 50% even at micromolar concentrations. Porcine brain natriuretic peptide (pBNP) binds with uniformly diminished affinity to all receptors, whereas the unrelated peptide, porcine vasoactive intestinal peptide, does not bind these receptors. The importance of the integrity of the ring structure of CNP is underlined by the significant loss of affinity when the peptide ring is opened.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial natriuretic peptide stimulates salt secretion by shark rectal gland by releasing VIP

1987 ◽  
Vol 252 (1) ◽  
pp. F99-F103 ◽  
Author(s):  
P. Silva ◽  
J. S. Stoff ◽  
R. J. Solomon ◽  
S. Lear ◽  
D. Kniaz ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Rectal Gland ◽  
Channel Blockers ◽  
Dogfish Shark ◽  
Local Release ◽  
Salt Secretion ◽  
Stimulation Of ◽  
Cardiac Peptides ◽  
Atrial Natriuretic

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.

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