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... It is similar in efficacy as secretin but slightly more potent than comparable stimulant as vasoactive intestinal polypeptide (VIP) [29,30]. Histamine can stimulate pancreatic juice secretion in the isolated dog pancreas [31], the anaesthetized dog [32,33], rabbit and guinea-pig [23,[34][35][36] but it is less effective as a secretagogue in the anaesthetized rat [37] and conscious dog [38]. In the in vitro pancreatic lobules of rabbit [28], segments of guinea pig [39,40] and rat [41] histamine can evoke marked increases in amylase secretion. ...
In addition to the autonomic nervous system and gut hormones, the mast cell mediator histamine has also been associated with exocrine pancreatic secretion. This review is concerned with the distribution and the physiological role of histamine in the control of pancreatic juice secretion. Histamine is distributed widely around blood vessels and acinar tissues in the pancreas and it is released in pancreatic juice during secretagogue stimulation. Histamine has a marked secretagogue effect in the exocrine pancreas of several animal species but in many cases the secretory effect is gender-related. The paracrine hormone exerts its secretory response via activation of H1 and H2 receptors on pancreatic acinar cells to mobilize potassium ions (K+) and cellular calcium (Ca2+) and through elevation of endogenous adenosine 3',5' cyclic monophosphate (cyclic AMP) levels, respectively. A physiological role for H3 receptors has also been associated with exocrine pancreatic secretion. H3 receptors are located presynaptically on parasympathetic nerve terminals to control the release of acetylcholine via restriction of Ca2+ access into nerve terminal through the N-type Ca2+ channel. Taken together, the results presented in this review strongly support histamine as a potential modulator of exocrine pancreatic function.
This study investigates the sex-related differences in pancreatic juice flow and total protein output in the isolated intact guinea-pig pancreas during infusion with either normal Krebs-Henseleit (KH) solution or optimal concentration of either histamine or its related receptor (H1, H2 and H3) agonists. Infusion of the pancreas with normal KH-solution had no significant effect on secretory parameters in male and female animals compared to basal. However, perfusion of the pancreas with optimal concentration (all 10-4 M) of either histamine (His), 2-thiazolylethylamine (2-TEA, H1 agonist), dimaprit (Dim, H2 agonist) or alpha-methylhistamine (alpha-MHis, H3 agonist) resulted in significant (p < 0.05) increases in pancreatic juice flow and total protein output in female and significant (p < 0.05) decreases in male animals compared to pre-stimulated basal values. Integration of the areas (arbitrary units) under the time course curves for each histaminergic agonist revealed significant elevation in secretory parameters in female and significant attenuation in male guinea-pigs. In contrast, when the results for male and female animals were combined they show no statistically significant difference in pancreatic juice flow and protein output compared to saline (K-H) infusion. These results indicate sex-related difference in histaminergic control of secretory parameters in the isolated guinea-pig pancreas. It is suggested that in future all results of exocrine pancreatic secretion in male and female animals should be analysed separately before presentation.
An investigation was made on the effects of histamine and related receptor agonists and antagonists on amylase secretion and Ca2+ mobilization in isolated guinea pig pancreatic segments and acinar cells. The effect of acetylcholine (ACh) was examined for comparison. Histamine evoked marked dose-dependent increases in amylase secretion and small changes in 45Ca2+ efflux, 45Ca2+ influx and intracellular free Ca2+ concentration [Ca2+]i, compared to much larger responses obtained with ACh. The H1 receptor agonist 2-thiazolyl-ethylamine (2-TEA) elicited a small increase in amylase secretion, whereas the H2 receptor agonist dimaprit had little or no effect. Similarly, 2-TEA evoked only small increases in Ca2+ mobilization, whereas dimaprit had no detectable effect. The H2 receptor antagonist oxmetidine also stimulated amylase output in a dose-dependent manner, similar in magnitude to histamine, whereas the H1 receptor antagonist chlorpheniramine (CPR) was only effective as a secretagogue at 10–2M The H1 antagonist also completely abolished the secretory responses of 2-TEA and markedly reduced the histamine-induced amylase secretion. The results demonstrate the involvement of histamine receptors in the control of amylase secretion and Ca2+ mobilization in guinea pig pancreatic acinar cells.Copyright © 1991 S. Karger AG, Basel
The effects of histamine alone and histamine plus cimetidine on basal pancreatic exocrine secretion were determined in anaesthetized rabbits with an acute pancreatic cannula. Intravenous histamine administration (0.2-0.8 n mol/kg/min) increased pancreatic enzyme secretion. A much greater stimulative effect on pancreatic secretion was observed when histamine was administered against a constant background of H2 antagonist (cimetidine 4 mumol/kg/min). The results indicate that in the rabbit pancreas the stimulatory effect of histamine is mediated by H1 receptors.
In dogs fitted with a pancreatic cannula and a duodenal cannula the intake of a standard meal induced a significant increase in the flow of pancreatic secretion and in the output of amylase, total protein, bicarbonate and chloride.
The oral administration (200 mg/day) of cimetidine to dogs was seen to elicit a marked decrease in postprandial flow increase and bicarbonate output, coinciding with a significant increase in amylase and total protein output. At the same time the postprandial duodenal pH remained at levels similar to those obtained in basal periods. The implications of secretin, gastrin and cholecystokinin (CCK) on these effects are discussed.
The use of H2-receptor agonists and antagonists allowed us to establish that histamine H2-receptors are present in pancreatic exocrine tissue and their stimulation caused a dose-dependent increase in pancreatic juice. The fact that H2-antagonists from one side and aminoguanidine from the other were unable to modify basal levels of pancreatic secretion, seems to minimize a role for H2-receptors in the regulation of pancreatic secretion. On the other hand H2-antagonists modified ceruletide-induced secretion in different ways according to the different molecules. Ranitidine strongly potentiated whereas cimetidine, oxmetidine and mifentidine slightly inhibited the effect of ceruletide. The stimulatory effect of eserine and the inhibitory effect of atropine indicate a cholinergic interference in the action of ceruletide. Therefore the potentiating effect of ranitidine may be related to its cholinomimetic action and the inhibitory effect of the other H2-antagonists may be connected with an anticholinergic effect. However, the potentiating effect of aminoguanidine on ceruletide-induced secretion may indicate a possible role for histamine in the response to ceruletide.
This study investigates the interaction between histamine and the adenylate cyclase systems involved in the secretion of amylase from the guinea-pig pancreatic lobules. Histamine increased amylase release, reaching a maximum response at 10(-5) M. Similarly, vasoactive intestinal peptide (VIP) evoked significant increase in amylase release, though not in a dose-dependent fashion. When the pancreatic lobules were incubated with histamine in combination with VIP, forskolin or 3-isobutyl-1-methylxanthine (IBMX), amylase secretion was increased as compared to histamine alone. The stimulatory effect of VIP was also increased by the presence of forskolin or IBMX. These findings suggest that in guinea-pig pancreatic lobules, VIP, forskolin and IBMX, agents involved in the cyclic adenosine monophosphate (cAMP) pathway, potentiate histamine stimulated amylase release.
The effects of histamine upon secretin- or cholecystokinin (CCK)-evoked exocrine pancreatic secretion were investigated in the anaesthetised guinea pig. Histamine (0.1 mumol/kg/min) induced a slight increase in pancreatic juice flow and total protein release compared to saline controls. Secretin (0.5 pmol/kg/min) and CCK-8 (0.75 pmol/kg/min) evoked marked time course increases in both the rate of pancreatic juice flow and total protein output in the anaesthetised guinea pig. Administration of either secretin or CCK-8 simultaneously with histamine elevated the exocrine pancreatic secretion compared to the smaller response obtained when administered separately. These results indicate that histamine may play an important physiological role in modulating the hormonal control of exocrine guinea pig pancreas.
An investigation was made of the effects of histamine on the K+ concentration in the effluent in superfused guinea pig and mouse pancreatic segments. The effect of acetylcholine (ACh) was examined for comparison. Histamine evoked a dose-dependent and transient increase in the K+ concentration in the effluent (K+ release) but is less potent compared to the cholinergic agonist, ACh. At the same doses histamine and ACh evoke a much larger K+ release from mouse superfused pancreatic segments followed in the poststimulus period by a reuptake of K+. However, this reuptake of K+ was not observed in guinea pig superfused pancreatic segments. On the other hand, the cholinergic antagonist, atropine, completely abolished the K+ release in response to ACh and histamine from mouse and guinea pig pancreatic segments. Our results show the involvement of histamine in the control of K+ release in pancreatic tissue, with significant differences in the observed responses between species.
The aim of this study was to investigate the possible involvement of the histamine H3 receptor in control of exocrine pancreatic secretion from the guinea-pig. In in vitro experiments, the H3 receptor agonist (R)-alpha-methylhistamine (0.01-10 microM) elicited a concentration-dependent decrease in the release of alpha-amylase. (R)-alpha-Methylhistamine concentrations above 10 microM evoked a concentration-dependent increase in alpha-amylase secretion. Application of mepyramine (1 microM) partially blocked this increase. The H3 receptor antagonist thioperanide (1 microM) blocked the effects of (R)-alpha-methylhistamine below 10 microM. Histamine and (R)-alpha-methylhistamine attenuated both protein release elicited during electrical-field stimulation and the release of tritiated choline, and these effects were reversed by thioperamide. In an in vivo study, (R)-alpha-methylhistamine increased juice secretion and total protein content of the juice by 40%. Histamine H1 and H2 receptor antagonists blocked this increase and uncovered an attenuation of the secretory parameters (juice flow 28%, total protein content 44%). This attenuation was blocked by thioperamide. These observations suggest that stimulation of the histamine H3 receptor in the pancreas results in a decreased fluid and enzyme release by inhibition of acetylcholine release from intrinsic pancreatic nerves.
1. This study investigates the interaction between histamine and the adenylate cyclase systems involved in the secretion of amylase in isolated guinea-pig pancreatic acinar cells. 2. Histamine caused does-related enhancement of amylase release. Similarly, incubation of acini with increasing concentrations of vasoactive intestinal peptide (VIP) resulted in a typical dose-dependent increase in amylase output. 3. When pancreatic acinar cells were incubated with histamine in combination with VIP, amylase secretion did not differ statistically from secretion induced by histamine or VIP alone and was significantly lower than theoretical additivity. Additionally, amylase secretion in the presence of histamine plus forskolin was significantly less than additive. The action of histamine was equally effective as VIP in causing cyclic adenosine monophosphate (cAMP) increase. 4. These results indicate that histamine may exert its secretory effects via the cyclic AMP pathway in the exocrine guinea-pig pancreas.
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