Somatostatin mediates bombesin inhibition of chloride secretion by rectal gland

1990 ◽  
Vol 258 (6) ◽  
pp. R1459-R1463
Author(s):  
P. Silva ◽  
S. Lear ◽  
S. Reichlin ◽  
F. H. Epstein
Keyword(s):  
Neurotransmitter Release ◽  
Fold Increase ◽  
Chloride Secretion ◽  
Inhibitory Effect ◽  
Nerve Fibers ◽  
Constant Infusion ◽  
Rectal Gland ◽  
Glandular Secretion ◽  
Rectal Glands

The function of bombesin-like peptide, a neurotransmitter present in nerve fibers of elasmobranch rectal glands, is unknown. Since the principal activity of the rectal gland is to secrete chloride, the effects of bombesin on chloride secretion and the role of somatostatin in this response was studied. Bombesin failed to stimulate secretion in rectal glands perfused in the basal state. When added to glands stimulated by a constant infusion of vasoactive intestinal peptide (VIP), bombesin (8 x 10(-7) M) reversibly inhibited chloride secretion by 56 +/- 9.7% and at the same time evoked a 10-fold increase in the liberation of somatostatin into the venous effluent. Inactivation of somatostatin by the addition of cysteamine partially suppressed the inhibitory effect of bombesin on glandular secretion. The effect of bombesin to reduce chloride secretion was completely prevented by the calcium channel blocker nifedipine, which inhibits neurotransmitter release. These results suggest that bombesin inhibits the effect of VIP to stimulate chloride secretion by releasing somatostatin from neurosecretory nerve terminals within the rectal gland.

scholarly journals Role of the Insulin-Like Growth Factor I Decline in the Induction of Atrogin-1/MAFbx during Fasting and Diabetes

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 4806-4812 ◽  
Author(s):  
Mischael Dehoux ◽  
Ronald Van Beneden ◽  
Nevi Pasko ◽  
Pascale Lause ◽  
Josiane Verniers ◽  
...  
Keyword(s):  
Growth Factor ◽  
Effective Dose ◽  
Fold Increase ◽  
Muscle Cells ◽  
Inhibitory Effect ◽  
Physiological Concentration ◽  
Igf I ◽  
Transcriptional Effect ◽  
The Relationship

Abstract In catabolic conditions, atrogin-1/MAFbx, a muscle-specific ubiquitin-ligase required for muscle atrophy, is increased, and concentrations of IGF-I, a growth factor known to have antiproteolytic action, are reduced. To define the relationship between the decline in IGF-I and the induction of atrogin-1/MAFbx, we studied the effect of IGF-I replacement on atrogin-1/MAFbx mRNA in rats fasted for 51 h and in rats made diabetic with streptozotocin (STZ). Fasting produced a 5.8-fold increase in atrogin-1/MAFbx (P < 0.001). This was attenuated to a 2.5-fold increase by injections of IGF-I (P < 0.05 vs. fasting). Animals with STZ-induced diabetes experienced a 15.1-fold increase in atrogin-1/MAFbx (P < 0.001). Normalization of their circulating IGF-I concentrations by IGF-I infusion blunted the induction of atrogin-1/MAFbx to 6.3-fold (P < 0.05 vs. STZ diabetes without IGF-I). To further delineate the regulation of atrogin-1/MAFbx by IGF-I, we studied a model of cultured muscle cells. We observed that IGF-I produced a time- and dose-dependent reduction of atrogin-1/MAFbx mRNA, with a 50% effective dose of 5 nm IGF-I, a physiological concentration. The degradation rate of atrogin-1/MAFbx mRNA was not affected by IGF-I, suggesting that the reduction of atrogin-1/MAFbx mRNA by IGF-I is a transcriptional effect. Exposure of muscle cells in culture to dexamethasone increased atrogin-1/MAFbx mRNA with a 50% effective dose of 10 nm, a pharmacological concentration. In the presence of dexamethasone, IGF-I at physiological concentrations retained its full inhibitory effect on atrogin-1/MAFbx mRNA. We conclude that IGF-I inhibits atrogin-1/MAFbx expression and speculate that this effect might contribute to the antiproteolytic action of IGF-I in muscle.

scholarly journals Mechanism and control of hyperosmotic NaCl-rich secretion by the rectal gland of Squalus acanthias

1983 ◽  
Vol 106 (1) ◽  
pp. 25-41 ◽  
Author(s):  
F. H. Epstein ◽  
J. S. Stoff ◽  
P. Silva
Keyword(s):  
Cyclic Amp ◽  
Chloride Secretion ◽  
Squalus Acanthias ◽  
Rectal Gland ◽  
Energetic Efficiency ◽  
Secondary Active Transport ◽  
Transport Pathway ◽  
Rectal Glands ◽  
And Control

Secretion of chloride from blood to lumen is accomplished in the rectal gland of elasmobranchs by a process of secondary active transport involving the co-transport of Cl- with Na+ across the basolateral membranes of rectal gland cells. Energy is provided by ATP via membrane Na-K-ATPase, which establishes an electrochemical gradient favouring Na+ influx into the cell. The involvement of K+ in the co-transport mechanism, so as to provide a ratio of 1 Na+:1 K+:2 Cl- entering the cell, would increase the energetic efficiency of the process, and is consistent with the Cl/O2 ration of 27–30 observed in secreting rectal glands. Secretion is stimulated by cyclic AMP (cAMP) and by vasoactive intestinal peptide (VIP) and adenosine, which activate adenylate cyclase. Activation of the gland in vivo probably occurs via VIP-secreting nerves as well as circulating agents; it is inhibited by somatostatin. Cyclic AMP probably stimulates chloride secretion by at least three mechanisms: (1) increasing chloride conductance across the luminal cell membrane, (2) enhancing the co-transport pathway for transmembrane movements of Na+, K+ and Cl- and (3) activating Na-K-ATPase.

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 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.

scholarly journals Sugar uptake, metabolism, and chloride secretion in the rectal gland of the spiny dogfish Squalus acanthias

2020 ◽  
Vol 319 (1) ◽  
pp. R96-R105
Author(s):  
Rolf Kinne ◽  
Katherine C. Spokes ◽  
Patricio Silva
Keyword(s):  
Glycogen Phosphorylase ◽  
Chloride Secretion ◽  
Squalus Acanthias ◽  
Rectal Gland ◽  
Sugar Uptake ◽  
Spiny Dogfish ◽  
Gland Cells ◽  
Exogenous Glucose ◽  
Glucose Transporter 2 ◽  
Rectal Glands

The rectal gland of the spiny dogfish Squalus acanthias secretes a salt solution isosmotic with plasma that maintains the salt homeostasis of the fish. It secretes salt against an electrochemical gradient that requires the expenditure of energy. Isolated rectal glands perfused without glucose secrete salt, albeit at a rate about 30% of glands perfused with 5 mM glucose. Gradually reducing the glucose concentration is associated with a progressive decrease in the secretion of chloride. The apparent Km for the exogenous glucose-dependent chloride secretion is around 2 mM. Phloretin and cytochalasin B, agents that inhibit facilitated glucose carriers of the solute carrier 2 (Slc2) family such as glucose transporter 2 (GLUT2), do not inhibit the secretion of chloride by the perfused rectal glands. Phloridzin, which inhibits Slc5 family of glucose symporters, or α-methyl-d-glucoside, which competitively inhibits the uptake of glucose through Slc5 symporters, inhibit the secretion of chloride. Thus the movement of glucose into the rectal gland cells appears to be mediated by a sodium-glucose symporter. Sodium-glucose cotransporter 1 (SGLT1), the first member of the Slc5 family of sodium-linked glucose symporters, was cloned from the rectal gland. No evidence of GLUT2 was found. The persistence of secretion of chloride in the absence of glucose in the perfusate suggests that there is an additional source of energy within the cells. The use of 2-mercapto-acetate did not result in any change in the secretion of chloride, suggesting that the oxidation of fatty acids is not the source of energy for the secretion of chloride. Perfusion of isolated glands with KCN in the absence of glucose further reduces the secretion of chloride but does not abolish it, again suggesting that there is another source of energy within the cells. Glucose was measured in the rectal gland cells and found to be at concentrations in the range of that in the perfusate. Glycogen measurements indicated that there are significant stores of glucose in the rectal gland. Moreover, glycogen synthase was partially cloned from rectal gland cells. The open reading frame of glycogen phosphorylase was also cloned from rectal gland cells. Measurements of glycogen phosphorylase showed that the enzyme is mostly in its active form in the cells. The cells of the rectal gland of the spiny dogfish require exogenous glucose to fully support the active secretion of salt. They have the means to transport glucose into the cells in the form of SGLT1. The cells also have an endogenous supply of glucose as glycogen and have the necessary elements to synthesize, store, and hydrolyze it.

Neural response of carotid chemoreceptors following dopamine blockade

1981 ◽  
Vol 50 (1) ◽  
pp. 172-177 ◽  
Author(s):  
D. F. Donnelly ◽  
E. J. Smith ◽  
R. E. Dutton
Keyword(s):  
Carotid Body ◽  
Inhibitory Effect ◽  
Neural Response ◽  
Nerve Fibers ◽  
Co2 Response ◽  
Blood Samples ◽  
Pentobarbital Sodium ◽  
Endogenous Dopamine ◽  
Air Discharge

The role of endogenous carotid body dopamine in the afferent chemoreceptor circuit was studied by means of haloperidol-induced dopamine antagonism. In 19 cats that were anesthetized with pentobarbital sodium and paralyzed, single carotid body nerve fibers were dissected free and placed on unipolar platinum wire electrodes. In 10 of these cats, the neural response to room air and the last 2 min of 6-min inhalations of 3, 6, and 9% CO2 were recorded, and blood samples were drawn for gas tension measurements. Haloperidol was administered at a dose (250 micrograms/kg) shown to block the inhibitory effect of injected dopamine. Following a 15-min equilibration, the CO2 response was again tested. In four other cats the CO2 response was tested with a hyperoxic background. In the remaining five cats the response to isocapnic hypoxia was recorded during administration of 15, 12, and 8% O2 before and following haloperidol. There was a significant increase in room air discharge activity and in hypoxic sensitivity following haloperidol. However, there was no significant change in hypercapnic sensitivity. These results suggest that there is a modulatory role for endogenous dopamine only in the hypoxic response.

Response Properties of Dural Nociceptors in Relation to Headache

2006 ◽  
Vol 95 (3) ◽  
pp. 1298-1306 ◽  
Author(s):  
Andrew M. Strassman ◽  
Dan Levy
Keyword(s):  
Sensory Neurons ◽  
Neurotransmitter Release ◽  
Inhibitory Effect ◽  
Mixed Effects ◽  
Electrophysiological Recording ◽  
Mechanical Stimuli ◽  
Nociceptive Neurons ◽  
Calcium Dependent ◽  
General Studies

Single-unit electrophysiological recording studies have examined the activity of sensory neurons in the trigeminal ganglion that innervate the intracranial meninges to better understand their possible role in headache. A key question is whether the meningeal sensory neurons are similar to nociceptive neurons in other tissues or, alternatively, whether they have unique properties that might be of significance for headache pathogenesis and drug therapy. Such studies have indeed found that the intracranial dura is innervated by neurons that exhibit properties characteristic of nociceptors in other tissues, including chemosensitivity and sensitization. This sensitization, consisting of an enhanced responsiveness to mechanical stimuli, might be relevant to symptoms that are characteristic of certain headaches that indicate the presence of an exaggerated intracranial mechanosensitivity. Studies that examined whether the anti-migraine agent sumatriptan might inhibit this sensitization (in addition to its well-known inhibition of neurotransmitter release) found that it had no inhibitory effect but rather produced a calcium-dependent discharge, which might account for the initial worsening of headache that can follow sumatriptan administration. In studies that examined the effects of vasodilator agents, nitroprusside produced mixed effects on mechanosensitivity, whereas calciton gene-related peptide (CGRP) had no effect on either spontaneous or mechanically evoked discharge. These results call into question the role of vasodilation in headache and suggest that the role of CGRP in headache may be through its action as a central neurotransmitter rather than through vasodilation and activation of meningeal nociceptors. In general, studies of meningeal sensory neurons have not found evidence of unique properties that distinguish them from nociceptive neurons in other tissues. Ultimately the distinctive clinical characteristics of headache may prove to be related not so much to any differences in the intrinsic molecular or cellular properties of the meningeal sensory neurons but rather to the distinctive properties of the tissue that they innervate.

Blood flow in the rectal gland of Squalus acanthias

1982 ◽  
Vol 243 (3) ◽  
pp. R296-R303 ◽  
Author(s):  
B. Kent ◽  
K. R. Olson
Keyword(s):  
Blood Flow ◽  
Microscopy Study ◽  
Electron Microscopy Study ◽  
Secretory Process ◽  
Rectal Gland ◽  
Rectal Glands ◽  
Arteries And Veins ◽  
Very High

The percent of cardiac output distributed to the rectal gland of 33 free-swimming fish was quantitated by the isotopically labeled microsphere technique. In 21 fish less than 1% was found in the rectal gland; 12 fish had 2-7%, suggesting a pattern of intermittent blood flow. Methylmethacrylate corrosion casts were made for scanning electron microscopy study of the microvasculature. Blood entering the rectal gland artery is distributed via three pathways. The most extensive is along the rectal gland artery into 11 or 12 circumferential vessels, which branch along the capsule and give rise to the radially arranged sinusoids that perfuse the secretory tubules and then join to form the central rectal gland vein. A second is an arterial bypass that runs the length of the rectal gland and joins the circulation of the postvalvular intestine. The third is via arteriovenous anastomoses in the capsule between tightly packed small arteries and veins. The low to moderate blood flow in most rectal glands and the very high flow in others is consistent with the observation that in vivo the rectal gland secretes only intermittently. Blood pathways allowing bypass of the rectal gland parenchyma suggest a role of blood flow in the regulation of the secretory process.

cGMP mediates effects of atrial peptides on medullary collecting duct cells

1987 ◽  
Vol 252 (3) ◽  
pp. F551-F559 ◽  
Author(s):  
M. L. Zeidel ◽  
P. Silva ◽  
B. M. Brenner ◽  
J. L. Seifter
Keyword(s):  
Collecting Duct ◽  
Renal Medulla ◽  
Fold Increase ◽  
Inhibitory Effect ◽  
Cyclic Monophosphate ◽  
Transport Effects ◽  
Collecting Duct Cells ◽  
Medullary Collecting Duct ◽  
Camp Levels

Atrial natriuretic peptides (ANP) stimulate renal Na+ excretion by poorly understood mechanisms, possibly involving direct inhibition of Na+ transport in the renal medulla. We have previously shown that human ANP 4-28 (hANP) inhibits Na+ entry-dependent O2 consumption (QO2) in rabbit inner medullary collecting duct (IMCD) cells. Because ANP actions in other tissues appear to be mediated by guanosine 3',5'-cyclic monophosphate (cGMP), the present studies examined the role of cyclic nucleotides in IMCD cell responses to ANP. 8-Bromo-cGMP (8-BrcGMP) diminished QO2 by 23.5 +/- 1.2% (SE) in IMCD cells but had no effect in cells derived from outer medullary collecting duct (OMCD); dibutyryl-adenosine 3',5'-cyclic monophosphate (cAMP) was without effect in IMCD cells. The inhibitory effect of BrcGMP was not additive with ANP, amiloride, or ouabain. Amphotericin, which enhances Na+ entry into cells, prevented the inhibitory effect of 8-BrcGMP. These results indicate that 8-BrcGMP, like ANP, inhibited Na+ entry in IMCD cells. hANP stimulated a 10-fold increase in cGMP in IMCD cells without altering IMCD cAMP levels or OMCD cGMP levels. Isobutyl methylxanthine, which inhibits phosphodiesterase activity, enhanced both cGMP accumulation and inhibition of QO2 by submaximal levels (10(-9) M) of ANP. Nitroprusside raised cGMP levels in both IMCD and OMCD cells but inhibited QO2 only in IMCD cells. We conclude that cGMP mediates the transport effects of ANP in IMCD cells. Our results indicate that cGMP may play an important role in the regulation of sodium transport in renal epithelia.

Oxytocin actions within the supraoptic and paraventricular nuclei: differential effects on peripheral and intranuclear vasopressin release

2006 ◽  
Vol 291 (1) ◽  
pp. R29-R36 ◽  
Author(s):  
Inga D. Neumann ◽  
Luz Torner ◽  
Nicola Toschi ◽  
Alexa H. Veenema
Keyword(s):  
Supraoptic Nucleus ◽  
Fold Increase ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Elevated Plasma ◽  
Acth Secretion ◽  
Vasopressin Release ◽  
Paraventricular Nuclei ◽  
Pituitary Adrenal Axis

In response to forced swimming (FS), AVP is released somato-dendritically within the supraoptic nucleus (SON) and paraventricular nucleus (PVN), but not from neurohypophyseal terminals into blood. Together with AVP, oxytocin (OXT) is released within the SON and PVN. Here, we studied the role of intra-SON and intra-PVN OXT in the regulation of local AVP release and into the blood in male rats. Within the SON, bilateral retrodialysis of an OXT receptor antagonist (OXT-A) increased local AVP release in response to FS [60 s, 21°C, vehicle twofold, not significant (ns); OXT-A: 15-fold increase, P < 0.05] without significantly affecting basal AVP release. In addition, local OXT-A elevated plasma AVP secretion under basal conditions (twofold increase, P < 0.05) without further elevation after FS. Within the PVN, exposure to FS elevated local AVP release, reaching significance only in the OXT-A group (vehicle: 1.4-fold, ns; OXT-A: 1.6-fold increase, P = 0.050). Bilateral OXT-A into the PVN did not affect peripheral AVP secretion either under basal or stress conditions. Basal ACTH concentrations tended to be elevated by local OXT-A within the PVN (1.7-fold increase, P = 0.076). In contrast, the swim-induced ACTH secretion was attenuated after retrodialysis of OXT-A within both the SON (at 5 min) and PVN (at 15 min) ( P < 0.05 both) compared with vehicle. The results demonstrate a receptor-mediated effect of OXT within the SON and PVN on local and neurohypophyseal AVP release, which depends upon the activity conditions. Further, while exerting an inhibitory effect on hypothalamo-pituitary-adrenal axis activity under basal conditions, hypothalamic OXT is essential for an adequate acute ACTH response.

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