Gastrin and somatostatin secretion by perfused rat stomach: functional linkage of antral peptides

1980 ◽  
Vol 238 (6) ◽  
pp. G495-G501 ◽  
Author(s):  
B. Saffouri ◽  
G. C. Weir ◽  
K. N. Bitar ◽  
G. M. Makhlouf
Keyword(s):  
Inverse Relationship ◽  
Rat Stomach ◽  
Gastrin Secretion ◽  
Functional Linkage ◽  
Somatostatin Secretion ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

The isolated vascularly perfused rat stomach was used to study the polarity, kinetics, and stoichiometry of gastrin and somatostatin secretion and the interaction of the two antral peptides. The secretion of gastrin (79%) and somatostatin (95%) was predominantly in the circulation. Methacholine (5 x 10(-8) to 5 x 10(-4) M) produced a biphasic dose-dependent increase in gastrin secretion. The maximal gastrin response (434 +/- 89% above basal levels; P less than 0.001) was partially inhibited by 10(-8) M atropine and completely inhibited by 10(-7) M atropine. Methacholine produced a dose-dependent inhibition of somatostatin secretion; the inhibition was blocked by atropine. An inverse relationship between the secretion of gastrin and somatostatin was noted in the basal state and during infusion of methacholine or prostaglandin E2; the latter had effects on gastrin and somatostatin secretion opposite to those of methacholine. The data, together with data reported elsewhere that somatostatin antiserum stimulates gastrin secretion in the perfused stomach, are consistent with the hypothesis that gastric somatostatin secretion exerts a continuous restraint on basal gastrin secretion and that stimulation of gastrin secretion may be mediated in part by inhibition of somatostatin secretion.

scholarly journals Proteoglycan and glycosaminoglycan synthesis in embryonic mouse salivary glands: effects of beta-D-xyloside, an inhibitor of branching morphogenesis.

1983 ◽  
Vol 96 (5) ◽  
pp. 1443-1450 ◽  
Author(s):  
H A Thompson ◽  
B S Spooner
Keyword(s):  
Salivary Glands ◽  
Dermatan Sulfate ◽  
Branching Morphogenesis ◽  
Proteoglycan Synthesis ◽  
Embryonic Mouse ◽  
Glycosaminoglycan Synthesis ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent ◽  
Stimulation Of

The proteoglycans and glycosaminoglycans synthesized by embryonic mouse salivary glands during normal morphogenesis and in the presence of beta-xyloside, an inhibitor of branching morphogenesis, have been partially characterized. Control and rho-nitrophenyl-beta-D-xyloside-treated salivary rudiments synthesize proteoglycans that are qualitatively similar, based on mobility on Sepharose CL-4B under dissociative conditions and glycosaminoglycan composition. However, beta-xyloside inhibits total proteoglycan-associated glycosaminoglycan synthesis by 50%, and also stimulates synthesis of large amounts of free chondroitin (dermatan) sulfate. This free glycosaminoglycan accounts for the threefold stimulation of total glycosaminoglycan synthesis in beta-xyloside-treated cultures. Several observations suggest that the disruption of proteoglycan synthesis rather than the presence of large amounts of free glycosaminoglycan is responsible for the inhibition of branching morphogenesis. (a) We have been unable to inhibit branching activity by adding large amounts of chondroitin (dermatan) sulfate, extracted from beta-xyloside-treated cultures, to the medium of salivary rudiments undergoing morphogenesis. (b) In the range of 0.1-0.4 mM beta-xyloside, the dose-dependent inhibition of branching morphogenesis is directly correlated with the inhibition of proteoglycan synthesis. The stimulation of free glycosaminoglycan synthesis is independent of dose in this range, since stimulation is maximal even at the lowest concentration used, 0.1 mM. The data strongly suggest that the inhibition of branching morphogenesis is caused by the disruption of proteoglycan synthesis in beta-xyloside-treated salivary glands.

Russell's viper venom stimulates insulin secretion from rat islets of Langerhans

1993 ◽  
Vol 136 (1) ◽  
pp. 27-33 ◽  
Author(s):  
P. M. Jones ◽  
F. M. Mann
Keyword(s):  
Insulin Secretion ◽  
Islets Of Langerhans ◽  
Prolonged Exposure ◽  
Blue Dye ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Russell’S Viper ◽  
Rat Islets Of Langerhans ◽  
Dose Dependent ◽  
Stimulation Of

ABSTRACT Burmese Russell's viper venom (RVV) caused a dose-and temperature-dependent stimulation of insulin secretion from islets of Langerhans isolated from rat pancreas by collagenase digestion. RVV stimulated both basal and glucose-induced insulin secretion at concentrations which did not compromise islet cell viability as assessed by exclusion of trypan blue dye. The effects of RVV on insulin secretion could not be attributed to the activation of protein kinase C (PKC), since down-regulation of PKC by prolonged exposure to a tumour-promoting phorbol ester did not abolish subsequent secretory responses to RVV. However, RVV-induced insulin secretion was inhibited in the absence of extracellular Ca2 +, and RVV did not stimulate insulin secretion from Ca2+-clamped electrically permeabilized islets at either substimulatory (50 nmol/l) or stimulatory (10 μmol/l) concentrations of Ca2 +, suggesting that changes in cytosolic Ca2+ are important in the stimulation of insulin secretion by RVV. The phospholipase A2 (PLA2) inhibitor quinacrine caused a dose-dependent inhibition of RVV-induced insulin secretion, suggesting that the activation of PLA2, perhaps in response to Ca2+ influx, may be partially responsible for RVV-induced insulin secretion. Journal of Endocrinology (1993) 136, 27–33

Enkephalinergic control of somatostatin secretion from the perfused rat stomach

1983 ◽  
Vol 61 (7) ◽  
pp. 657-663 ◽  
Author(s):  
C. H. S. McIntosh ◽  
Y. N. Kwok ◽  
T. Mordhorst ◽  
E. Nishimura ◽  
R. A. Pederson ◽  
...  
Keyword(s):  
Vagal Stimulation ◽  
Gastric Inhibitory Polypeptide ◽  
Endogenous Opioids ◽  
Rat Stomach ◽  
Basal Secretion ◽  
Dependent Inhibition ◽  
Order Of Magnitude ◽  
Endogenous Enkephalins ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

A role for the enkephalins in the regulation of gastric somatostatin (SLI) secretion has been investigated in an isolated perfused rat stomach model. Both methionine- and leucine-enkephalins caused a dose-dependent inhibition of gastric inhibitory polypeptide (GIP) stimulated SLI secretion. Leu-enkephalin was one order of magnitude less potent than met-enkephalin: 50% inhibition by met-enkephalin was at 4 × 10−9 M and with leu-enkephalin 3.5 × 10−8 M. Naloxone (100 nM) had no effect on basal secretion but blocked the inhibitory action of met-enkephalin (1 nM or 1 μM). Vagal stimulation (7 V, 10 Hz, 5 ms) inhibited GIP-stimulated SLI release. Administration of naloxone partially reversed this inhibition, suggesting that endogenous opioids were at least partially responsible for vagally induced inhibition. A number of possible pathways by which endogenous enkephalins may modulate SLI release have been proposed.

Stimulation of gastrin and somatostatin secretion from the isolated rat stomach by bombesin

1981 ◽  
Vol 241 (3) ◽  
pp. G242-G247 ◽  
Author(s):  
J. W. DuVal ◽  
B. Saffouri ◽  
G. C. Weir ◽  
J. H. Walsh ◽  
A. Arimura ◽  
...  
Keyword(s):  
Maximal Response ◽  
Antral Mucosa ◽  
Rat Stomach ◽  
Peak Period ◽  
Cellular Origin ◽  
Gastrin Secretion ◽  
Somatostatin Secretion ◽  
D Cells ◽  
Dose Dependent Increase

The role of bombesin in the regulation of gastrin and somatostatin secretion was examined using an isolated vascularly perfused rat stomach preparation. Bombesin caused a biphasic, dose-dependent increase in gastrin and bombesin secretion. Neither somatostatin nor gastrin secretion was inhibited by atropine. The maximal gastrin response to bombesin (198 +/- 75% above basal levels) was less than one-half the maximal response to methacholine (462 +/- 94%). It was postulated that the concomitant release of somatostatin, in part from antral mucosa, attenuated the gastrin response to bombesin; the notion was tested with somatostatin antiserum. A 50- to 100-fold excess of sheep somatostatin antiserum augmented significantly the maximal gastrin response to bombesin by 966% in the initial peak period and by 532% in the plateau period; the response in the plateau period was not significantly different from the maximal response to methacholine. Methacholine stimulated the release of gastric bombesin also, but the exact cellular origin of the peptide could not be ascertained. On the basis of these results and of the topography of antral bombesin neurons and somatostatin D cells, a model for the neural (via bombesin) and paracrine (via somatostatin) control of gastrin secretion within the antrum is proposed.

scholarly journals The role of GTP in prostaglandin E1 stimulation of adenylate cyclase in platelet membranes

1983 ◽  
Vol 214 (1) ◽  
pp. 231-234 ◽  
Author(s):  
J M Stein ◽  
B R Martin
Keyword(s):  
Adenylate Cyclase ◽  
Prostaglandin E1 ◽  
Platelet Membrane ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent ◽  
Stimulation Of

Adenylate cyclase activity in platelet membrane preparations was measured in the presence of prostaglandin E1 (PGE1), GTP and a non-hydrolysable analogue of GDP, guanosine 5′-[beta-thio]diphosphate (GDP[beta S]). A dose-dependent inhibition of adenylate cyclase by GDP[beta S] was observed that could be reversed either by adding increased amounts of GTP or of PGE1.

Effects of colchicine and vinblastine on in vitro gastric secretion.

1979 ◽  
Vol 236 (5) ◽  
pp. E550
Author(s):  
D K Kasbekar ◽  
G S Gordon
Keyword(s):  
Gastric Secretion ◽  
Cytochalasin B ◽  
Pepsinogen Secretion ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Kinetics Of ◽  
Dose Dependent ◽  
Kinetics Of Inhibition ◽  
Stimulation Of

The effects of colchicine and vinblastine on in vitro bullfrog gastric mucosal preparations were studied with respect to H+ and pepsinogen secretion. In the concentration range of 1--50 mM, an initial but transient colchicine-mediated stimulation of H+ secretion is followed by a dose-dependent inhibition. The transient stimulation of H+ secretion can be confirmed in resting preparations in the absence of added secretagogues. In the same concentration range, colchicine inhibits pepsinogen secretion to a greater degree than H+ secretion. Vinblastine (10(-5)--5 X 10(-4) M) was more effective than colchicine in inhibiting both H+ and pepsinogen secretion. The kinetics of inhibition of secretion by both colchicine and vinblastine were slow. Cytochalasin B had no effect on either secretion.

Regulation of gastrin and somatostatin secretion by cholinergic and noncholinergic intramural neurons

1982 ◽  
Vol 243 (6) ◽  
pp. G442-G447 ◽  
Author(s):  
M. L. Schubert ◽  
K. N. Bitar ◽  
G. M. Makhlouf
Keyword(s):  
Electrical Stimulation ◽  
Cholinergic Neuron ◽  
Maximal Response ◽  
Rat Stomach ◽  
Gastrin Secretion ◽  
Somatostatin Secretion ◽  
Stimulation Of

The regulation of gastrin and somatostatin secretion by intramural neurons was examined in the isolated vascularly perfused rat stomach. The optimal modalities of transmural electrical stimulation of the antrum were established to be 40 V and 10 Hz. Stimulation at increasing cycle durations (0.1-4 ms) caused increasing gastrin secretion that was progressively more resistant to atropine. The maximal gastrin response to 4-ms cycles was equal to the maximal response to methacholine. However, the response to methacholine was inhibited 70-90% by atropine, whereas the response to 4-ms cycles was inhibited by 15% only. Stimulation at all cycle durations caused a decrease in somatostatin secretion. Atropine converted the decrease to an increase, from which it was concluded that before atropine somatostatin secretion was the net result of cholinergic inhibition and noncholinergic stimulation of somatostatin. The results indicate that cholinergic and noncholinergic intramural neurons are predominantly but not exclusively activated by 0.1- and 4-ms cycles, respectively. The existence of distinct neurons was supported by results of stimulation of preganglionic vagal fibers with 0.2- and 4-ms cycles. The findings are consistent with a model according to which gastrin secretion is regulated by two interdependent intramural neurons: a cholinergic neuron that stimulates gastrin secretion indirectly by inhibition of somatostatin secretion and a noncholinergic neuron that stimulates gastrin secretion directly by release of a peptide stimulant, probably bombesin.

Paracrine regulation of gastric acid secretion by fundic somatostatin

1987 ◽  
Vol 252 (4) ◽  
pp. G485-G490 ◽  
Author(s):  
M. L. Schubert ◽  
N. F. Edwards ◽  
A. Arimura ◽  
G. M. Makhlouf
Keyword(s):  
Acid Secretion ◽  
Normal Serum ◽  
Field Stimulation ◽  
Cholinergic Stimulation ◽  
Somatostatin Secretion ◽  
Somatostatin Cells ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Cholinergic Effect ◽  
Stimulation Of

The isolated, luminally perfused mouse stomach was used to determine whether somatostatin cells located in proximity to parietal cells exert a paracrine influence on acid secretion. Acid secretion in response to histamine and pentagastrin was accompanied by a dose-dependent increase in somatostatin secretion. Incubation of the stomach with somatostatin antiserum (final dilution 1:100), but not with normal serum, augmented significantly basal and secretagogue-stimulated acid secretion. The augmentation was most evident with submaximal stimuli (92 +/- 18%, P less than 0.01, with 15 microM pentagastrin and 160 +/- 6%, P less than 0.001, with 5 microM histamine) and least evident with maximal stimuli (30 +/- 12%, P less than 0.05, with 200 microM histamine). The acid response to submaximal field stimulation (10 V, 20 Hz, 0.5 ms), which was accompanied by an increase in somatostatin secretion, was also augmented by somatostatin antiserum (115 +/- 12%, P less than 0.01), whereas the response to maximal field stimulation (20 V, 20 Hz, 0.5 ms), which was accompanied by a decrease in somatostatin secretion, a typically cholinergic effect, was not augmented further. It is concluded that fundic somatostatin modulates the acid secretory response to paracrine (histamine), hormonal (gastrin), and neural (acetylcholine) stimuli and that cholinergic stimulation of acid secretion reflects both the direct effect of acetylcholine on the parietal cell and its ability to eliminate the paracrine restraint exerted by somatostatin.

scholarly journals CXCL9 and CXCL11 Chemokines Modulation by Peroxisome Proliferator-Activated Receptor-α Agonists Secretion in Graves’ and Normal Thyrocytes

2010 ◽  
Vol 95 (12) ◽  
pp. E413-E420 ◽  
Author(s):  
Alessandro Antonelli ◽  
Silvia Martina Ferrari ◽  
Silvia Frascerra ◽  
Cinzia Pupilli ◽  
Caterina Mancusi ◽  
...  
Keyword(s):  
Peroxisome Proliferator ◽  
Thyroid Cells ◽  
Peroxisome Proliferator Activated Receptor ◽  
Dependent Inhibition ◽  
Pparγ Agonists ◽  
Dose Dependent Inhibition ◽  
And Control ◽  
Dose Dependent ◽  
Stimulation Of

Context: Peroxisome proliferator-activated receptor (PPAR)-α has been shown to exert immunomodulatory effects in autoimmune disorders. However, until now, no data were present in the literature about the effect of PPARα activation on CXCL9 and CXCL11 chemokines in general or on secretion of these chemokines in thyroid cells. Objective and Design: The presence of PPARα and PPARγ has been evaluated by real-time-PCR in Graves’ disease (GD) and control cells in primary culture. Furthermore, we have tested the role of PPARα and PPARγ activation on CXCL9 and CXCL11 secretion in GD and control cells after stimulation of these chemokines secretion with IFNγ and TNFα. Results: This study shows the presence of PPARα and PPARγ in GD and control cells. A potent dose-dependent inhibition by PPARα-agonists was observed on the cytokines-stimulated secretion of CXCL9 and CXCL11 in GD and control cells. The potency of the PPARα agonists used was maximum on the secretion of CXCL9, reaching about 90% of inhibition by fenofibrate and 85% by ciprofibrate. The relative potency of the compounds was different with each chemokine; for example, gemfibrozil exerted a 55% inhibition on CXCL11, whereas it had a weaker activity on CXCL9 (40% inhibition). PPARα agonists were stronger (ANOVA, P < 0.001) inhibitors of CXCL9 and CXCL11 secretion in thyrocytes than PPARγ agonists. Conclusions: Our study shows the presence of PPARα in GD and control thyrocytes. PPARα activators are potent inhibitors of the secretion of CXCL9 and CXCL11, suggesting that PPARα may be involved in the modulation of the immune response in the thyroid.

Differences between antigenic determinants of pig and cat zona pellucida proteins

Reproduction ◽  
2000 ◽  
pp. 15-23 ◽  
Author(s):  
K Jewgenow ◽  
M Rohleder ◽  
I Wegner
Keyword(s):  
In Vitro Fertilization ◽  
Zona Pellucida ◽  
Antigenic Determinants ◽  
Vitro Fertilization ◽  
Contraceptive Vaccine ◽  
Sperm Binding ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

Despite many efforts, the control of reproduction in feral cat populations is still a problem in urban regions around the world. Immunocontraception is a promising approach; thus the present study examined the suitability of the widely used pig zona pellucida proteins (pZP) for contraception in feral domestic cats. Purified zona pellucida proteins obtained from pig and cat ovaries were used to produce highly specific antisera in rabbits. Antibodies against pZP raised in rabbits or lions were not effective inhibitors of either in vitro sperm binding (cat spermatozoa to cat oocytes) or in vitro fertilization in cats, whereas antibodies against feline zona pellucida proteins (fZP) raised in rabbits showed a dose-dependent inhibition of in vitro fertilization. Immunoelectrophoresis, ELISA and immunohistology of ovaries confirmed these results, showing crossreactivity of anti-fZP sera to fZP and to a lesser extent to pZP, but no interaction of anti-pZP sera with fZP. It is concluded that cat and pig zonae pellucidae express a very small number of shared antigenic determinants, making the use of pZP vaccine in cats questionable. A contraceptive vaccine based on feline zona pellucida determinants will be a better choice for the control of reproduction in feral cats if immunogenity can be achieved.

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