Cholinergic and adrenergic control of enzyme secretion in isolated rat pancreas

Varga, Gábor; Papp, M.; Vizi, E.S.

doi:10.1007/bf01536926

Cited by 11 publications

(8 citation statements)

References 14 publications

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“…The results indicate that the enhancing effect of EFS on pancreatic exocrine secretion is mediated by activation of intrapancreatic neurons, mainly cholinergic neurons. The partial inhibition of EFSevoked pancreatic exocrine secretion by atropine was also observed in studies of the isolated perfused rat pancreas [28] as well as isolated segments of the guinea pig and the rat pancreas [30,38]. The incomplete inhibition by atropine suggests that EFS may also activate noncholinergic excitatory neurons, including peptidergic [3], serotonergic [17] and adrenergic [23] excitatory neurons, in the pancreas.…”

Section: Discussionmentioning

confidence: 66%

Effects of intrapancreatic neuronal activation on cholecystokinin-induced exocrine secretion of isolated perfused rat pancreas

Park¹,

Park

Lee³

et al. 1999

Pfl�gers Archiv European Journal of Physiology

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The role of intrapancreatic neurons in the action of cholecystokinin (CCK) on pancreatic exocrine secretion of the totally isolated, perfused rat pancreas was investigated. Intrapancreatic neurons were activated by applying electrical field stimulation (EFS) to the isolated pancreas for 45 min. When applying EFS, spontaneous pancreatic secretions of fluid and amylase increased until the second 15-min period of EFS and then decreased during the third 15-min period. Atropine (2 microM) notably reduced the EFS-evoked pancreatic secretions of fluid and amylase. The CCK-induced (10 pM) pancreatic secretions of fluid and amylase elevated further in the first 15-min period of EFS and then gradually resumed to the levels observed during application of CCK alone in the third 15-min period of EFS. However, the CCK-induced pancreatic secretions remained elevated even in the third 15-min period of EFS when an action of endogenous somatostatin was inhibited by cyclo-(7-aminoheptanonyl-Phe-d-Trp-Lys-Thr[BZL]) (10 nM) or pertussis toxin (200 ng/ml). EFS further elevated spontaneous exocrine secretion by the cysteamine-treated (300 mg/kg) pancreas, but this was markedly reduced, to normal levels, by infusing somatostatin (100 pM). EFS increased the numbers of immunoreactive somatostatin cells in the Langerhans' islets. The results indicate that intrapancreatic neuronal activation influences CCK-induced pancreatic secretions in a dual-phase pattern in the rat: an increase during the early phase and a decrease during the late phase. Endogenous somatostatin released from the islets appears to inhibit the enhancing effect of neuronal activation on CCK-induced pancreatic secretion. Of the intrapancreatic neurons, the cholinergic ones appear to predominate in EFS's effects on CCK-induced pancreatic secretion.

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Section: Discussionmentioning

confidence: 66%

Effects of intrapancreatic neuronal activation on cholecystokinin-induced exocrine secretion of isolated perfused rat pancreas

Park¹,

Park

Lee³

et al. 1999

Pfl�gers Archiv European Journal of Physiology

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“…This has been thought to be a result of the release of beta-adrenergic agonists from the nerves in the pancreas. The EFS-induced increase in amylase release has been shown to be Ca 2+ -dependent [20,21].…”

Section: Introductionmentioning

confidence: 99%

“…This introduction shows that EFS has several effects on cells in addition to the well known property of neurotransmitter release enhancement in neuronal profiles. Although the role of EFS on exocrine secretion of the pancreas has been widely investigated [8,20,21], the effects of EFS on insulin and glucagon secretion from the endocrine pancreas of normal and diabetic rats have not yet been investigated. This study examined the effect of EFS alone and in combination with either atropine (a cholinergic muscarinic receptor antagonist) or propranolol (a b-adrenergic receptor antagonist) or yohimbine (an a2-adrenergic receptor antagonist) or tetrodotoxin (an inhibitor of action potential in excitable tissues) on insulin and glucagon secretion from the in vitro pancreatic tissue fragments of normal and diabetic rats.…”

Section: Introductionmentioning

confidence: 99%

Effect of Electrical Field Stimulation on Insulin and Glucagon Secretion from the Pancreas of Normal and Diabetic Rats

Adeghate

Ponery²,

Wahab³

2001

Horm Metab Res

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The effect of electrical field stimulation (EFS) on insulin (INS) and glucagon (GLU) secretion from normal and diabetic rat pancreas is poorly understood. In our study, EFS (5-20Hz, 50 V amplitude and 1.0 ms pulse width), when applied alone, resulted in a significant (p<0.05) increase in INS secretion from the pancreas of both normal and diabetic rats. Atropine (10(-5) M) did not inhibit the EFS (5 Hz)-evoked INS secretion in normal pancreas and failed to alter the effect of EFS (10-20 Hz) on INS secretion from the pancreas of both normal and diabetic rats. Propranolol (Prop) inhibited INS secretion to below basal level in the presence of EFS (5 Hz) but not at EFS (10- 20 Hz). Tetrodotoxin (TTX) also significantly (p = 0.002) inhibited INS secretion from normal pancreas in the presence of EFS (5-20 Hz). The decrease in insulin secretion observed when pancreatic tissue fragments were incubated in Prop and TTX in the presence of EFS was reversed by yohimbine (10(-5) M). In contrast, TTX did not significantly modify INS secretion from diabetic pancreas in the presence of EFS. EFS (5-20 Hz) significantly (p<0.05) increased GLU release from normal and diabetic rat pancreas when applied alone. Neither atropine, Prop nor TTX significantly modified GLU release from the pancreas of either normal or diabetic rats. This suggests that GLU secretion may be controlled through a different pathway. The EFS-evoked INS and GLU secretion is probably executed via different mechanisms. These mechanisms include 1) activation of cholinergic nerves by EFS; 2) EFS of alpha- and beta-adrenergic nerves; 3) activation of non-adrenergic non-cholinergic pathway by EFS; 4) EFS-induced depolarization and subsequent action potential in pancreatic endocrine cells and 5) electroporosity caused by EFS-induced membrane permeability. All of these effects may be summative. In conclusion, EFS (5-20 Hz), when applied alone, can evoke significant increases in INS and GLU secretion from the pancreas of both normal and diabetic rats. Insulin secretion is controlled via alpha-2 adrenergic (inhibition) and beta-adrenergic (stimulation) receptors. Glucagon secretion is enhanced by alpha2 adrenergic stimulation.

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“…THE IMPORTANCE OF INTRAPANCREATIC noncholinergic excitatory neurons in pancreatic exocrine function has been proposed because atropine does not completely block pancreatic secretion induced by vagal stimulation (8,19) or intrapancreatic neuronal excitation (17,23,31). In a recent study (22), we demonstrated that activation of intrapancreatic neurons by electrical field stimulation (EFS) results in a further increase in secretin-induced pancreatic exocrine secretion of the isolated rat pancreas.…”

mentioning

confidence: 96%

Role of GRPergic neurons in secretin-evoked exocrine secretion in isolated rat pancreas

Park

Kwon

Lee

et al. 2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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Effects of intrapancreatic gastrin-releasing peptide (GRP)-containing neurons on secretin-induced pancreatic secretion were investigated in the totally isolated perfused rat pancreas. Electrical field stimulation (EFS) increased secretin (12 pM)-induced pancreatic secretions of fluid and amylase. EFS induced a twofold increase in GRP concentration in portal effluent, which was completely inhibited by tetrodotoxin but not modified by atropine. An anti-GRP antiserum inhibited the EFS-enhanced secretin-induced secretions of fluid and amylase by 12 and 43%, respectively, whereas a simultaneous infusion of the antiserum and atropine completely abolished them. Exogenous GRP dose-dependently increased the secretin-induced pancreatic secretion with an additive effect on fluid secretion and a potentiating effect on amylase secretion, which was not affected by atropine. In conclusion, excitation by EFS of GRPergic neurons in the isolated rat pancreas results in the release of GRP, which exerts an additive effect on fluid secretion and a potentiating effect on amylase secretion stimulated by secretin. The release and action of GRP in the rat pancreas are independent of cholinergic tone.

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Cholinergic and adrenergic control of enzyme secretion in isolated rat pancreas

Cited by 11 publications

References 14 publications

Effects of intrapancreatic neuronal activation on cholecystokinin-induced exocrine secretion of isolated perfused rat pancreas

Effects of intrapancreatic neuronal activation on cholecystokinin-induced exocrine secretion of isolated perfused rat pancreas

Effect of Electrical Field Stimulation on Insulin and Glucagon Secretion from the Pancreas of Normal and Diabetic Rats

Role of GRPergic neurons in secretin-evoked exocrine secretion in isolated rat pancreas

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