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J J Calvo

Publications and source records attributed to J J Calvo.

At least 19 recordsLinked to original sources
PubMed1996

Impairment of intracellular calcium homoeostasis in the exocrine pancreas after caerulein-induced acute pancreatitis in the rat.

1. We have measured intracellular calcium concentrations in basal conditions and in response to cholecystokinin-octapeptide and acetylcholine in pancreatic acini isolated from rats with caerulein-induced acute pancreatitis and compared them with those in control rats. 2. We also measured amylase secretion in basal conditions and in response to cholecystokinin-octapeptide in both groups. 3. In pancreatic acini from rats with pancreatitis the basal intracellular calcium concentration was significantly increased (134.9 +/- 7.1 nmol/l compared with 71.8 +/- 2.9 nmol/l, P < 0.001). Moreover, the maximum values of intracellular calcium attained during the stimulation period were equivalent in acini from control and pancreatitic rats with no statistically significant differences. 4. In acini from control rats the differences between the resting levels of intracellular calcium and the maximum intracellular calcium values (delta[Ca2+]i) in response to several concentrations of cholecystokinin-octapeptide showed a clear dose-response relationship, with a half-maximal increase at 0.1 nmol/l and a maximal difference (delta[Ca2+]i = 259 +/- 50 nmol/l) at 1 nmol/l. In contrast, a right-shifted response, with a statistically significant smaller increase, was observed in acini from pancreatitic rats. 5. Basal amylase release was significantly higher in acini from rats with pancreatitis (11.7 +/- 1.0% of total compared with 5.9 +/- 1.1% of total, P < 0.001). In contrast, cholecystokinin-octapeptide and acetyl-choline-evoked amylase secretion was reduced by more than 85% in acini from pancreatitic rats. 6. In conclusion, calcium homoeostasis in pancreatic acinar cells from rats with caerulein-induced pancreatitis seems to be impaired. These results suggest excessive release of acinar free ionized calcium, or damage to the integrity of mechanisms that restore low resting levels of intracellular free ionized calcium, and the consequent calcium toxicity could be the key trigger in caerulein-induced acute pancreatitis.

Acetylcholine↗
PubMed1995

Description of an automated method for the in vitro measurement of trypsinogen secretion from pancreatic segments.

The characterization of trypsinogen output from superfused pancreatic tissue by an automated spectrophotometric method is described. To test the method we investigated the time-course and the dose-response curve for acetylcholine-induced trypsinogen release from superfused pancreatic segments. We have demonstrated that this method allows the on-line detection and estimation of trypsinogen release with suitability, stability, and sensitivity.

Acetylcholine↗
PubMed1995

Effect of adenosine and adenosine agonists on amylase release from rat pancreatic lobules.

The effects of adenosine on the amylase secretion from rat pancreatic lobules have been studied. Adenosine induces a dose-dependent stimulation on amylase release, which is maximal at a concentration of 10(-4) M. It has been observed a clear inhibition of this secretory action when atropine was added whereas no amylase release was seen in isolated acini after adenosine. The effect of adenosine is completely blocked by the adenosine receptors antagonist theophylline (10(-4) M), but not by dipyridamole (10(-3) M), a drug that inhibits the transport of adenosine into the cell. The increase of amylase secretion induced by adenosine is inhibited by either the relatively selective A1 receptor antagonist PD116,948 (10(-6) M) and by the A2 receptor antagonist PD115,199 (10(-6) M). Significant increases of amylase release are observed after the relatively selective A1 receptor agonist R-PIA (10(-5) M) and after the relatively selective A2 receptor agonist NECA (10(-4) M). Finally, the effect of R-PIA is not modified by coincubation with PD115,199 and the effect of NECA is not affected by coincubation with PD116,948. These results suggest that the action of adenosine is mediated through the release of acetylcholine and probably by the simultaneous occupation of both A1 and A2 adenosine receptors, whereas the intracellular action of adenosine could be discarded.

Adenosine↗
PubMed1995

Heterogeneous decrease of bone mineral density in the vertebral column of ovariectomized rats.

The long-term effect of ovariectomy on the loss of bone mineral density (BMD) was evaluated in rats with and without estrogen treatment; BMD was studied in the lumbar and caudal vertebrae, measured by DXA, to find how the losses of BMD occur in the axial skeleton. Seventy female Wistar rats of 3 months of age were divided into four groups as follows: group 1: control animals; group 2: ovariectomized animals; group 3: ovariectomized animals undergoing treatment with estrogen (0.25 mg/kg per week of 17-beta estradiol); group 4: ovariectomized rats undergoing estrogen treatment only during the last 3 months of the experimental period. No significant differences were found among the groups in regard to the BMD values of the caudal vertebrae at either 3 or 6 months. Likewise, in the lumbar vertebrae there were no significant differences among the groups after 3 months. However, at 6 months, a decrease in the BMDs of the ovariectomized animals with respect to the remaining groups was found: 226 +/- 11 mg/cm2 in the ovariectomized group; 262 +/- 14 mg/cm2 in the controls; 255 +/- 4 mg/cm2 in the rats receiving estrogen treatment for 6 months; and 259 +/- 5 mg/cm2 in the animals receiving estrogen for 3 months. The study also reveals the absence of differences in the bone mineral density between the ovariectomized and control rats when the former received estrogen treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗
PubMed1995

Cholinergic pathways are involved in secretin and VIP release and the exocrine pancreatic response after intraduodenally perfused acetic and lactic acids in the rat.

The response of the exocrine pancreas to intraduodenal perfusion of acetic and lactic acids in normal and previously atropinized rats was studied. Secretin and vasoactive intestinal peptide (VIP) plasma levels in portal plasma were also measured. Intraduodenal perfusion of both acetic and lactic acids significantly stimulated flow rate (from 0.29 +/- 0.03 microliters/min to a maximum of 1.06 +/- 0.08 microliters/min after acetic and from 0.35 +/- 0.05 microliters/min to a maximum of 1.13 +/- 0.12 microliters/min after lactic acid perfusion) and protein output (from 11.16 +/- 2.33 micrograms/min to a maximum of 35.1 +/- 7.4 micrograms/min after acetic and from 8.98 +/- 0.95 micrograms/min to a maximum of 22.5 +/- 1.3 micrograms/min after lactic acid perfusion). Atropine treatment significantly inhibited pancreatic flow rate and protein output after acetic acid perfusion, but no inhibition of flow rate and a slight decrease in the protein output after lactic acid perfusion were seen. With respect to plasma peptide concentrations, significant increases in secretin and VIP levels were found after perfusion of both organic acids; atropine administration significantly decreased plasma secretin levels after acetic acid administration although it did not affect plasma VIP concentrations. By contrast, atropine significantly increased plasma secretin levels, but significantly lower values of plasma VIP concentrations were observed after lactic acid perfusion. Therefore, cholinergic mechanisms are involved in the release of secretin and VIP and different types of control of exocrine pancreatic secretion occur, depending on the features of the intraduodenal stimulant.

Acetates↗
PubMed1995

Dose-response effects of VIP on the rabbit exocrine pancreatic secretion. Comparison with PACAP-27 actions.

A dose-response study of the effects of vasoactive intestinal peptide (VIP) on the exocrine pancreatic secretion of the rabbit has been made. Furthermore, the actions of VIP and pituitary adenylate cyclase activating peptide (PACAP) on the exocrine pancreatic secretion were compared at a similar molar dose. After the infusion of VIP a linear dose-response relationship for pancreatic flow rate and bicarbonate output, up to the dose of 4 micrograms/kg, was observed. VIP acts as a partial agonist of secretin, the rabbit pancreas being less sensitive to VIP compared with other mammals. Moreover, VIP did not significantly stimulate the pancreatic protein output. PACAP stimulated the hydroelectrolyte fraction of the exocrine pancreatic secretion in a similar manner to that of VIP. Unlike what was observed with VIP, PACAP, on the same molar basis, significantly stimulated the protein and amylase outputs. Furthermore, PACAP releases VIP, so that the action of PACAP on the hydroelectrolyte fraction may be partially mediated by VIP; on the other hand, VIP is not involved in the effect of PACAP on the pancreatic enzyme secretion of this species.

Amylases↗
PubMed1994

Platelet-activating factor mediates pancreatic function derangement in caerulein-induced pancreatitis in rats.

1. We have assessed the role of platelet-activating factor in caerulein-induced acute pancreatitis (four subcutaneous injections of caerulein at a dose of 20 micrograms/kg) by measuring platelet-activating factor levels in portal blood, pancreatic tissue and peritoneal exudate in rats with and without pancreatitis. 2. We have also observed the effect of the platelet-activating factor antagonist, BN-52021, on the hyperamylasaemia and exocrine pancreatic secretion impairment associated with pancreatitis. 3. In rats with pancreatitis the basal pancreatic flow rate was increased (1.63 +/- 0.41 versus 0.25 +/- 0.03 microliters/min). Total protein output was similar in both untreated (5.98 +/- 1.93 micrograms/min) and caerulein-injected (6.5 +/- 2.0 micrograms/min) animals. Amylase output was lower in rats with pancreatitis (19.6 +/- 4.8 mu-units/min) than in controls (39.4 +/- 16.6 mu-units/min). 4. Caerulein-treated animals had significantly higher serum amylase levels than untreated animals. BN-52021 significantly reduced the caerulein-induced hyperamylasaemia. 5. Portal blood platelet-activating factor levels increased in rats with pancreatitis and in rats infused with cholecystokinin. Rats injected with caerulein and BN-52021 had portal blood levels of platelet-activating factor that were lower than those with pancreatitis. 6. Morphological derangements associated with pancreatitis (inflammatory infiltration and cell vacuolization) were also markedly reduced in BN-52021-treated animals. 7. The results of this study suggest that platelet-activating factor is involved in the development of caerulein-induced acute pancreatitis in rats.

Acute Disease↗
PubMed1994

Comparison between the effects of VIP and the novel peptide PACAP on the exocrine pancreatic secretion of the rat.

The effect of intravenous infusion of pituitary adenylate cyclase-activating peptide (PACAP) 27, a novel regulatory peptide that shows a close structural and chemical similarity to vasoactive intestinal peptide (VIP), on the rat exocrine pancreatic secretion was studied. PACAP and VIP stimulated the flow rate of exocrine pancreatic secretion (p < 0.05). However, protein output and amylase secretion were mainly stimulated by PACAP. Intravenous infusion of VIP increased the plasma levels of secretin (p < 0.05). On the other hand, PACAP released neither secretin nor VIP. Our results show: (a) both PACAP and VIP stimulate exocrine pancreatic secretion, (b) PACAP stimulation of pancreatic amylase and protein secretion is greater than that induced by VIP, and (c) PACAP probably exerts a direct effect on exocrine pancreas whereas some of the actions of VIP might be mediated by secretin.

Amylases↗
PubMed1994

Effects of acute intravenous ethanol on basal exocrine pancreatic secretion in rat: cholinergic involvement.

The effect of intravenous infusion of ethanol on the basal exocrine pancreatic secretion of anesthetized rats was studied. The cholinergic involvement on the actions of ethanol was also studied using previously atropinized animals. During the stimulation period, pancreatic flow rate was significantly increased by intravenous ethanol in both un-atropinized (199% compared with basal) and atropinized rats (195% compared with basal). Pancreatic protein output was also increased during ethanol administration in both groups of animals (171% and 165% compared with basal in, respectively, un-atropinized and atropinized rats). After the administration of ethanol, in the poststimulation period, pancreatic flow rate was further increased only in the atropinized group of rats (290% compared with basal), whose values were significantly higher than those of ethanol-treated un-atropinized animals (195% compared with basal). A similar profile of response was observed in pancreatic protein output. Since intravenous ethanol did not stimulate either secretin or VIP release to portal plasma, the present results point to a direct effect of this substance on the exocrine pancreas. Furthermore, atropine revealed the existence of an inhibitory cholinergic effect of ethanol on the exocrine pancreas. In summary, results show that the effect of intravenous ethanol on the basal exocrine pancreatic secretion is dual and antagonistic.

Acetylcholine↗
PubMed1993

Exocrine pancreatic response to intraduodenal fatty acids and fats in rabbits.

1. The exocrine pancreatic secretion in rabbits after intraduodenal perfusion of, respectively, a short-chain fatty acid (propionate), a long-chain fatty acid (oleate) and a neutral fat (intralipid) has been studied. 2. Only the neutral fat and the long-chain fatty acid stimulated the hydroelectrolyte fraction of exocrine pancreatic secretion in a dose-related fashion, but this response was not mediated by secretin release. 3. Acinar secretion was more effectively stimulated after propionate perfusion than by oleate and this was governed by different mechanisms. 4. Neutral fat, without predigestion, stimulated the pancreatic enzyme secretion in the rabbit.

Animals↗
PubMed1993

Nicotinic cholinergic influences in pancreatic secretion induced by intraduodenal alkaline and acid solutions in the rabbit.

1. The effect of hexamethonium on the exocrine pancreatic response to intraduodenal acidification and alkalinization, and the secretin and VIP release after these stimuli, was studied. 2. The hydroelectrolyte secretion after hydrochloric acid and sodium carbonate perfusion was reduced by hexamethonium treated (322 +/- 44% of maximum response in flow rate to sodium carbonate perfusion in untreated animals vs 140 +/- 12% in pretreated animals, and 252 +/- 19% of maximum response in flow rate to HCl in untreated animals vs 166 +/- 11% in pretreated animals). 3. However, hexamethonium has no effect on secretin plasma levels after either intraduodenal acidification or alkalinization. 4. On the contrary, the ganglion blocker significantly (P < 0.01) reduced plasma VIP levels in response to intraduodenal HCl (maximum response 320 +/- 74% in untreated vs 184 +/- 44% in hexamethonium-treated animals). 5. Plasma VIP levels showed a similar increase in both untreated (maximum response: 151 +/- 12%) and ganglion blocked animals (170 +/- 26%) in response to sodium carbonate. 6. These data suggest the existence of complex neural mechanisms in the exocrine pancreatic response to intraduodenal stimuli, these mechanisms being different depending on the intraduodenal stimulus.

Acids↗
PubMed1993

Mechanisms involved in the control of exocrine pancreatic secretion in the interdigestive state in the rabbit.

The effect of rapid wash-out of the duodenum with phosphate buffered saline on exocrine pancreatic secretion and plasma levels of secretin, VIP, gastrin and CCK was studied. Furthermore, the possible nervous role in this effect was checked after atropine and hexamethonium treatment. Rapid wash-out significantly increased protein output (35.0 micrograms/min, in the control group without duodenal perfusion and 72.15 micrograms/min, in the perfused group) and the plasma levels of CCK (from 5.2 to 13.17 fmol/ml). Intravenous infusion of atropine significantly reduced the protein output (from 78.19 to 32.45 micrograms/min) and the plasma levels of CCK (from 10.1 to 5.55 fmol/ml), with no change in the remaining parameters in the intraduodenally perfused group. Intravenous administration of hexamethonium significantly stimulated hydroelectrolyte secretion (from 6.99 to 15.15 microliters/min) and the plasma levels of VIP (from 4.8 to 7.3 fmol/ml) and reduced the protein output (from 61.47 to 30.75 micrograms/min) and the plasma levels of CCK (from 14.56 to 6.25 fmol/ml) in the intraduodenally perfused group. Our results suggest that, in the interdigestive state, the exocrine pancreatic secretion of the rabbit is tonically inhibited. This inhibition can be divided into two different mechanisms: on the one hand there is a decrease in enzyme secretion produced by a duodenal factor and mediated by CCK and muscarinic mechanisms and on the other, there is an inhibition of hydroelectrolyte secretion with no duodenal participation which is probably controlled by nervous non-muscarinic mechanisms and VIP involvement.

Animals↗
PubMed1992

Cholinergic mechanisms for secretin release after intraduodenal alkalinization in the anaesthetized rabbit.

Exocrine pancreatic response to duodenal perfusion with alkaline solutions (pH 11.4) was studied in the anaesthetized rabbit; secretin and vasoactive intestinal polypeptide (VIP) levels in portal plasma were measured and the contribution of cholinergic mechanisms was also evaluated. Intraduodenal perfusion of sodium carbonate stimulated flow rate and bicarbonate output to a maximum of 322 +/- 44 and 609 +/- 105% respectively compared with basal levels. Significant increases of plasma secretin levels, with a maximum of 267 +/- 38% as compared with basal, were also observed. A lower increase in VIP levels (maximum of 151 +/- 12%) was seen. All these effects, except the VIP response, were substantially inhibited by atropine. Our results show that exocrine pancreatic response to intraduodenal sodium carbonate is specifically focused on hydroelectrolytic secretion. Keeping in mind what occurs after intraduodenal alkaline phosphate buffer administration (at the same pH as sodium carbonate: 11.4) it seems that about 50% of the pancreatic response to sodium carbonate may be ascribed to pH and the remaining 50% to the carbonate anion. Moreover, this response would mainly be mediated by secretin, whose release can be facilitated by a cholinergic reflex.

Alkalies↗
PubMed1992

Effect of intraduodenal sodium bicarbonate in rat and rabbit exocrine pancreatic secretion.

The effect of intraduodenal sodium bicarbonate, 0.1 M, on exocrine pancreatic secretion and the release of two peptides, secretin and VIP, was studied in anesthetized rats and rabbits, two species largely used in the gastroenterology laboratories. In the rabbit, intraduodenal sodium bicarbonate perfusion had no effect either on exocrine pancreatic secretion or on portal plasma levels of secretin and VIP. By contrast, in the rat, intraduodenal sodium bicarbonate perfusion significantly increased hydroelectrolyte exocrine pancreatic secretion and portal plasma secretin levels. A clear interspecific difference reflecting the different gastrointestinal physiology of both species is observed.

Animals↗
PubMed1992

Cholinergic mechanisms involved in the effect of intraduodenal ethanol on exocrine pancreatic secretion.

The effect of intraduodenal ethanol on exocrine pancreas of the rat in basal conditions has been studied. The pancreatic flow rate significantly increased to a maximum of 148% of basal after intraduodenal ethanol whereas only slight increases of protein output were observed. Ethanol perfusion in previously atropinized animals also elicited a significant increase of the flow rate up to a maximum of 177% of basal values but this increase appeared later than that observed in non-atropinized animals. Our results show that the ethanol action is successively stimulant followed by a simultaneously dual and antagonic effect (stimulant and inhibitory). Furthermore, this ethanol effect is mediated by cholinergic mechanisms. Finally, no effect of ethanol on portal plasma secretin and VIP levels was observed in atropinized or non-atropinized animals.

Animals↗
PubMed1991

Pancreatic dose dependent effect of intraduodenal HCl in the anesthetized rabbit.

1. A dose-response relationship between intraduodenal perfusion of different HCl loads (1.8, 4.5, 9, 18 and 45 mmol/hr) and volume, bicarbonate and protein outputs, from the exocrine pancreas of anaesthetized rabbits was observed. 2. This study also shows a dose-response relationship between the different HCl loads and the porta levels of secretin and VIP. 3. The secretin response showed a marked decrease during the stimulation period and this may suggest the involvement of a neural mechanism. 4. The plasma VIP responses were of a magnitude that might suggest a hormone role for VIP in this effect.

Animals↗
PubMed1990

Acinar cholecystokinin (CCK) receptors in the exocrine pancreas of the rat: effect of adrenalectomy.

The binding of [125I]BH-CCK-8 to membranes of acinar cells from rats at 6 and 21 days after adrenalectomy was studied. The optimum conditions of time and temperature were previously established as being 120 min and 30 degrees C. Under these conditions, the membranes of the adrenalectomized animals of both groups (6 and 21 days) bound more radioligand than those from control rats. However, a qualitative study of the binding showed that the affinities of binding were much lower; in particular, the high affinity receptors had a Kd of 0.94 +/- 0.33 nM in the controls and this was 14.9 +/- 1.29 nM in the 6-day adrenalectomized animals, although the maximum binding capacity did not vary significantly. However, in the case of the low affinity receptors, there was a gradual increase in the maximum binding capacity as the time after adrenalectomy progressed: 717 +/- 121, 1,987 +/- 183, and 10,175 +/- 862 fmol/mg for the control, 6-day, and 21-day adrenalectomized rats, respectively. In the latter situation, the high affinity receptors completely disappeared. These results, which coincide with a marked deficit in protein secretion already described in adrenalectomized rats, can be accounted for in terms of the possible negative cooperativity exerted by the low affinity receptors on the high affinity hormone-receptor complex, the protein secretion of the acinar cells normally mediated by the high affinity receptors becoming paralyzed.

Adrenalectomy↗