Adrenergic nervous control of cAMP-mediated amylase secretion in the rat pancreas

Pearson, Gemma; Singh, J.; Petersen, O. H.

doi:10.1152/ajpgi.1984.246.5.g563

Cited by 26 publications

(42 citation statements)

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“…These observations corroborate several other findings (Adeghate & Donàth, 1990, 1991. In addition to the classical neurotransmitters (ACh and NA) which innervate the pancreas (Lenninger, 1974;Pearson et al 1984) it is now well established that the pancreas is also innervated by peptidergic nerves which release several neuropeptides including CCK, substance P, neuropeptide Y, vasoactive intestinal polypeptide and several others (Adeghate & Donàth, 1990;Holst, 1993;Adeghate et al 1997). The results of this study have confirmed the presence of CCK-immunopositive nerves in the endocrine pancreas and around blood vessels of normal and diabetic animals.…”

Section: Immunohistochemistrysupporting

confidence: 86%

“…The secretion of pancreatic juice is controlled mainly by the autonomic nervous system (Lenninger, 1974;Pearson et al 1984) and by the two naturally occurring gut hormones, secretin and cholecystokinin (Chey, 1993). More recently, other substances including the islet hormones, vasoactive intestinal polypeptide (VIP), phorbol esters, nitric oxide, histamine and the growth hormones have been implicated in the regulation of exocrine pancreatic secretion (Pearson et al 1982;Singh, 1985a;Nishizuka, 1988;Owyang, 1993;Williams & Goldfine, 1993;Lajas et al 1996;Singh et al 1997).…”

Section: Introductionmentioning

confidence: 99%

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Interaction of Islet Hormones with Cholecystokinin Octapeptide‐Evoked Secretory Responses in the Isolated Pancreas of Normal and Diabetic Rats

Singh

Adeghate

Salido

et al. 1999

Experimental Physiology

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summaryThis study investigates the effects of the islet hormones, insulin (Ins), glucagon (Glu) and somatostatin (Som) with cholecystokinin octapeptide (CCK-8) on amylase secretion and intracellular free calcium concentration [Ca¥]é and their pattern of distribution in the isolated pancreas of normal and diabetic rats. Ins and Glu evoked small increases in amylase output from pancreatic segments compared with a much enhanced effect of CCK-8. In contrast, Som induced a biphasic response comprising an initial decrease followed by a secondary increase and this biphasic response may be dependent upon the concentration. Combining the islet hormones with CCK-8 resulted in marked potentiation in amylase output compared with either CCK-8 alone or the individual hormone. Genistein and tyrphostin A25, the tyrosine kinase inhibitors, evoked a small decrease in amylase output from pancreatic segments. They had no effect on the CCK-8-evoked secretory response but markedly inhibited the potentiation of the islet hormones with CCK-8. In pancreatic acini and acinar cells Ins, Glu and Som individually evoked small increases in amylase output compared with a much larger response with CCK-8. When the islet hormones were combined with CCK-8 there was no potentiation of amylase output. Similarly, when rats were rendered diabetic by prior treatment with streptozotocin Ins, Glu and Som failed to potentiate the secretory response of CCK-8. In fura_2-loaded pancreatic acinar cells Ins or Glu evoked small increases in [Ca¥]é compared with a much larger elevation with CCK-8. Ins, Glu and Som each enhanced the CCK-8-evoked [Ca¥]é. Genistein elicited a decrease in [Ca¥]é both in the absence and presence of the islet hormones. It also decreased the elevation in [Ca¥]é resulting from the combined presence of CCK-8 with either Ins or Glu but it had no effect on CCK-8 in combination with Som. In pancreatic acinar cells from diabetic rat Ins, Glu and Som had no detectable effect on CCK-8-evoked elevation in [Ca¥]é compared with the response obtained with CCK-8 alone. CCK-8-immunopositive cells were distributed around the walls of blood vessels, numerous Inspositive cells in the central and peripheral parts of the islets of Langerhans, Glu-immunoreactive cells in the periphery of islets and Som-positive cells in the outer part of the islets. During diabetes, the number of CCK-immunopositive cells remained unchanged whereas the number of Inspositive cells decreased coupled with an increase in the number of Glu-positive cells. The results indicate that both tyrosine kinase and cellular Ca¥ seem to be the intracellular mediators involved with the enhanced secretory responses obtained with a combination of the islet hormones with CCK-8. Moreover, the presence of viable pancreatic islets of Langerhans seems to be associated with the potentiation of the islet hormones with CCK-8.

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Section: Immunohistochemistrysupporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Interaction of Islet Hormones with Cholecystokinin Octapeptide‐Evoked Secretory Responses in the Isolated Pancreas of Normal and Diabetic Rats

Singh

Adeghate

Salido

et al. 1999

Experimental Physiology

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“…Experiments were performed according to the method of Pearson et al (1984), with minor modifications. were killed by a blow to the head and the pancreas was quickly removed and placed in a modified Krebs-Henseleit solution of the following composition (mM): NaCl 103, KCI 4.7, CaCl2 2.56, MgCl2 1.13, NaHCO3 25, NaH2PO4 1.15, D-glucose 2.8, sodium pyruvate 4.9, sodium fumarate 2.7, and sodium glutamate 4.9.…”

Section: In Vitro Experimentsmentioning

confidence: 99%

Effect of a new potent CCK antagonist, lorglumide, on caerulein‐ and bombesin‐induced pancreatic secretion and growth in the rat

Scarpignato

Varga

Dobronyi

et al. 1989

British J Pharmacology

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1 The effect of lorglumide, a new potent cholecystokinin (CCK) antagonist, on pancreatic secretion and growth induced by caerulein and bombesin was studied in the rat. 2 Pancreatic exocrine secretion was studied both in vitro (isolated and perfused pancreatic segments) and in vivo (anaesthetized animals with cannulation of the common bile duct) whereas the trophic effect was investiged after short-term (5 days) administration of the peptides and/or lorglumide. 3 Both caerulein and bombesin stimulated amylase release from in vitro pancreatic segments in a concentration-dependent manner. Although the efficacy of both peptides was virtually identical, the potency of caerulein was higher than that of bombesin. Lorglumide displaced the concentrationresponse curves to caerulein to the right without affecting the maximum response, suggesting a competitive antagonism. The Schild plot analysis of data gave a straight line with a slope not significantly different from unity. The calculated pA2 for lorglumide was 7.31 + 0.45. The antagonist, however, was completely ineffective when tested against bombesin-induced amylase release. 4 In vivo experiments confirmed results from in vitro studies since lorglumide (5 and I0mgkg 1) significantly reduced pancreatic exocrine secretion induced by caerulein without affecting the response to bombesin. 5 Administration of either peptide increased the weight of the pancreas, the total pancreatic protein and DNA, trypsin and amylase content. Lorglumide (10mgkg-1), administered together with caerulein, reduced the peptide-induced increase in pancreatic weight, protein and enzyme content. On the contrary, when lorglumide was given together with bombesin, all the parameters that were examined were not altered by concomitant administration of the antagonist. 6 These results have demonstrated the ability of lorglumide to antagonize the effects on the pancreas of a CCK-analogue, caerulein, and its inability to affect bombesin-induced pancreatic secretion and growth, suggesting that lorglumide is a potent and selective antagonist of CCK-receptors in the pancreas.

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“…Interestingly, in the same series of experiments atropine completely blocked the secretory response evoked by ACh and markedly reduced the amylase output elicited by EFS. The failure of atropine to abolish the effect of EFS completely is not strange, since in the rat pancreas part of the nerve-mediated secretory response is due to a sympathetic component (Pearson et al 1984). Furthermore, it is unlikely that secretin is acting to inhibit the release of ACh during EFS, since the gut hormone can also attenuate the secretagogue effect of exogenous application of ACh.…”

Section: Discussionmentioning

confidence: 99%

“…The technique of electrical field stimulation has been shown previously to be a useful and effective physiological tool for activating intrinsic nerves in the in vitro pancreas to study the effect of endogenous neurotransmitters on pancreatic secretion (Davison et al 1980;Pearson et al 1984). This present study has also shown that stimulation of intrinsic secretomotor nerves in the isolated rat pancreas can result in marked increases in amylase secretion, which are associated with an elevation in cytosolic free Ca2" concentration, radiolabelled Ca2" influx and a net efflux of Mg2".…”

Section: Discussionmentioning

confidence: 99%

Interaction between secretin and nerve‐mediated amylase secretion in the isolated exocrine rat pancreas

Wisdom¹,

Camello²,

Salido³

et al. 1994

Experimental Physiology

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SUMMARYThis study investigates the effects of the gut peptide, secretin, on nerve-mediated and acetylcholine-evoked amylase secretion and calcium (Ca2") and magnesium (Mg2") mobilization in the in vitro rat pancreas. Both electrical field stimulation (EFS; 50 V, 20 Hz, 1 ms) and acetylcholine (ACh; 10-6 M) caused marked increases in amylase output in isolated pancreatic segments. These responses were inhibited by atropine (10-`M). Secretin (10-'°and 108 M) evoked only a small increase in amylase secretion, which was unaffected by atropine. Combining either EFS or ACh with secretin resulted in an attenuation in amylase output compared with the response obtained with either EFS or ACh alone. In a Mg2"-free medium, secretin failed to inhibit the amylase output evoked by EFS. When forskolin (10-5M) was combined with EFS there was a marked potentiation of amylase output. In fura-2-loaded acinar cells, ACh (10-6 M)

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Adrenergic nervous control of cAMP-mediated amylase secretion in the rat pancreas

Cited by 26 publications

References 0 publications

Interaction of Islet Hormones with Cholecystokinin Octapeptide‐Evoked Secretory Responses in the Isolated Pancreas of Normal and Diabetic Rats

Interaction of Islet Hormones with Cholecystokinin Octapeptide‐Evoked Secretory Responses in the Isolated Pancreas of Normal and Diabetic Rats

Effect of a new potent CCK antagonist, lorglumide, on caerulein‐ and bombesin‐induced pancreatic secretion and growth in the rat

Interaction between secretin and nerve‐mediated amylase secretion in the isolated exocrine rat pancreas

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