Action of cholera toxin on dispersed acini from guinea pig pancreas

Gardner, Jerry D.; Rottman, Alvin J.

doi:10.1016/0304-4165(79)90025-4

Cited by 30 publications

(6 citation statements)

References 30 publications

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“…It has also become recognized that vasoactive intestinal polypeptide (VIP) and the hormone secretin, which act on target cells via cyclic AMP, as well as pharmacologic agents which increase cyclic AMP, such as cholera toxin, theophylline and 3-isobutyl-1-methyl xanthine, stimulate secretion in some species such as guinea-pig but not in others (Heisler, Grondin & Forget, 1974; Deschodt-Lanckman, Robberecht, DeNeef, Labrie & Christophe, 1975;Smith & Case, 1975;Bauduin, Stock, Launay, Vincent, Potvliege & Grenier, 1977;Gardner & Jackson, 1977;Robberecht, Deschodt-Lanckman, Lammens, DeNeef & Christophe, 1977;Gardner & Rottman, 1979). In mouse pancreas especially, agonists working via cyclic AMP have little or no effect on amylase secretion.…”

Section: Introductionmentioning

confidence: 99%

Interaction of cholecystokinin and vasoactive intestinal polypeptide on function of mouse pancreatic acini in vitro.

Burnham¹,

McChesney²,

Thurston³

et al. 1984

The Journal of Physiology

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SUMMARY1. In isolated mouse pancreatic acini, vasoactive intestinal polypeptide (VIP) and secretin potentiated amylase release stimulated by cholecystokinin (CCK). VIP (1-100 nM) or secretin (100-1000 nM) alone elicited a negligible secretary response, whereas in combination with CCK, these agents induced a significantly larger response.2. VIP increased maximal amylase release elicited by CCK without affecting the potency with which CCK stimulated secretion.3. The phosphodiesterase inhibitor, 3-isobutyl-1-methyl xanthine (IBMX), from 0-03-1-0 mM had effects on secretion similar to those of VIP. VIP, IBMX and 8-Br-cyclic AMP, all of which act through or mimic the action of cyclic AMP, potentiated the secretary response to maximal concentrations of CCK, carbamylcholine and the ionophore A23187, all of which act via intracellular calcium.4. In contrast to amylase release, stimulation of acinar glucose transport by CCK or carbamylcholine was not augmented by VIP, secretin, IBMX or 8-Br-cyclic AMP.5. The results indicate that for amylase release from mouse pancreas, secretagogues acting via cyclic AMP potentiate those acting via calcium. However, potentiation does not apply to all biological responses of the pancreatic acinus and each response must be studied individually.

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Section: Introductionmentioning

confidence: 99%

Interaction of cholecystokinin and vasoactive intestinal polypeptide on function of mouse pancreatic acini in vitro.

Burnham¹,

McChesney²,

Thurston³

et al. 1984

The Journal of Physiology

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“…(3) Effects of choiera toxin on kinetic parameters of rat pancreatic adenylate cyclase A choiera toxin pretreatment increases cychc AMP levels in the intact rat pancréas [35,36] and in dispersed acini from guinea-pig pancréas [37]. This effect in intact ceUs probably corresponds to the 13fold increased efficacy of GTP on adenylate cyclase documented here after a pretreatment with 30 ^g/m\ choiera toxin (Table I).…”

Section: (2) Comparison Of the Values Of Kinetic Parameters In Rat Pamentioning

confidence: 60%

Distinct effects of the C-terminal octapeptide of cholecystokinin and of a cholera toxin pretreatment on the kinetics of rat pancreatic adenylate cyclase activity

Svoboda

Lambert

Christophe

1981

Biochimica et Biophysica Acta (BBA) - General Subjects

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(1) The kinetic parameters of rat pancreatic adenylate cyclase were evaluated, using GTP, p[NH]ppG or GTP gamma S as nucleotide activator, cholecystokinin as peptide hormone, and GDP beta S and dibutyryl cyclic GMP as inhibitors of guanosine triphosphate and CCK-8, respectively. The time courses of activation and the degree of activation at steady state (EA/ETOT) were compatible with a simple two-state model of activation-deactivation based on a pseudo-monomolecular activation process (rate constant kappa+1), and a deactivation process (rate constant kappa off) that included, depending on the activating nucleotide, the hydrolysis of GTP (rate constant kappa 2) and/or the dissociation of the intact nucleotide (rate constant kappa-1), so that EA/ETOT = kappa+1/(kappa+1 + kappa 2 + kappa-1). (2) The hormone CCK-8 increased the value of kappa+1 with GTP dose-dependently, from 0.2 to 10.9 min-1. The value of kappa-1 increased 0.01 to 0.3 min-1 but the value of kappa 2 was unaltered at 7 min-1, so that EA/ETOT increased 15-fold, from 4% to 61%. (3) A cholera toxin pretreatment at 30 micrograms/ml allowed also a large increase in EA/ETOT with GTP (up to 51%) but the underlying mechanism was different. It consisted of a 14-fold decrease in the kappa off value of the GTP-activated enzyme (from 7 min-1 to 0.5 min-1) that corresponded to a reduction in GTPase activity. When testing the system with p[NH]ppG, two added effects of the cholera toxin pretreatment were observed: a 4-fold increase in the value of kappa+1 (from 0.2 to 0.8 min-1) and the occurrence of a significant 0.3 min-1 value for kappa-1.

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“…In the guinea-pig pancreas, secretin, vasoactive intestinal polypeptide (VIP) and cholera toxin were reported to increase cellular cyclic AMP and stimulate enzyme secretion (Gardner, Conlon & Adams, 1976; Robberecht, Conlon & Gardner, 1976;Gardner & Jackson, 1977;Gardner & Rottman, 1979). Gardner & Jackson (1977) postulated that cyclic AMP (elaborated by acinar cells or contaminating duct cells) was involved in one of the major pathways for the regulation of digestive enzyme secretion from pancreatic acinar cells.…”

Section: Introductionmentioning

confidence: 99%

Role of cyclic adenosine monophosphate in amylase release from dissociated rat pancreatic acini

Singh

1982

The Journal of Physiology

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SUMMARY1. The effect ofoctapeptide of cholecystokinin-pancreozymin (CCK8), bethanechol, cholera toxin, glucagon and vasoactive intestinal polypeptide (VIP) on amylase secretion and lactic dehydrogenase (LDH) release from isolated rat pancreatic acini was studied.2. In isolated rat pancreatic acini, in the absence of theophylline in the medium, amylase secretion was increased by 65-78 % with 10-7 and 10-6 M-cholera toxin. In the presence of theophylline, amylase secretion was increased by 43-56 % with 10-7 and 10-6 M-cholera toxin following a 90 min incubation. No effect was observed in the presence of theophylline at 30 and 60 min. The effect of cholera toxin was potentiated by CCK8 at 60 and 90 min.3. In the absence of theophylline in the medium, amylase secretion was increased by 81-118 % with 10-5 and 10-4 M-glucagon and 86 % with 10-6 M-VIP at 60 min. In the presence of theophylline in the medium, amylase secretion was increased by 53-246% with 10-9 to 10-6M-glucagon and 111-158% with 10-7 and 10-6 M-VIP respectively. The effect of glucagon and VIP was potentiated by CCK8.4. Potentiation of the rate of amylase release due to glucagon (10-5 M) and VIP (10-6 M) occurred during the first 15 min of incubation.5. Release of LDH was not increased by any of these agents. 6. It is concluded that cyclic AMP rise (due to cholera toxin, glucagon and VIP effect) increased amylase secretion from rat pancreatic acinar cells. This effect is less marked than in the guinea-pig pancreas and is potentiated by agents mobilizing cellular Ca2+ (CCK8 and bethanechol).7. These data indicate species-specific variation in the action of cyclic AMP in the pancreas.

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Action of cholera toxin on dispersed acini from guinea pig pancreas

Cited by 30 publications

References 30 publications

Interaction of cholecystokinin and vasoactive intestinal polypeptide on function of mouse pancreatic acini in vitro.

Interaction of cholecystokinin and vasoactive intestinal polypeptide on function of mouse pancreatic acini in vitro.

Distinct effects of the C-terminal octapeptide of cholecystokinin and of a cholera toxin pretreatment on the kinetics of rat pancreatic adenylate cyclase activity

Role of cyclic adenosine monophosphate in amylase release from dissociated rat pancreatic acini

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