Vasoactive intestinal polypeptide in vagally mediated pancreatic secretion of fluid and HCO3.

Fahrenkrug, Jan; Muckadell, Ove B. Schaffalitzky de; Holst, Jens J.; Jensen, S. L.

doi:10.1152/ajpendo.1979.237.6.e535

Cited by 39 publications

(20 citation statements)

References 14 publications

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“…5C), which suggests the existence of other inhibitory neurotransmitters. Indeed, other inhibitory neurotransmitters, such as ATP, vasoactive intestinal polypeptide, ␤-nicotinamide adenine dinucleotide, hydrogen sulfide, and carbon monoxide, have been reported (Burnstock et al, 1970;Fahrenkrug et al, 1979;Miller et al, 2001;MutafovaYambolieva et al, 2007;Linden et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Involvement of TRPV2 Activation in Intestinal Movement through Nitric Oxide Production in Mice

Mihara¹,

Boudaka²,

Shibasaki³

et al. 2010

J. Neurosci.

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Transient receptor potential channel vanilloid 2 (TRPV2) can detect various stimuli such as temperature (Ͼ52°C), stretch, and chemicals, including 2-aminoethoxydiphenyl borate, probenecid, and lysophospholipids. Although expressed in many tissues, including sensory and motor neurons, TRPV2 expression and function in the gastrointestinal tract is poorly understood. Here, we show TRPV2 expression in the murine intestine and its involvement in intestinal function. Almost all mouse intestinal intrinsic sensory and inhibitory motor neurons, both cell bodies and nerve fibers, showed TRPV2 immunoreactivity. Several known TRPV2 activators increased cytosolic Ca 2ϩ concentrations and evoked TRPV2-like current responses in dissociated myenteric neurons. Interestingly, mechanical stimuli activated inward currents in a strength-dependent manner, which were inhibited by a TRPV2 inhibitor tranilast. TRPV2 activation in isolated intestine inhibited spontaneous circular muscle contraction, which did not occur in the presence of the TRPV2 antagonist, tetrodotoxin or nitro oxide (NO) synthase pathway inhibitors. Also, increased intestinal NO production was observed in response to a TRPV2 agonist, and gastrointestinal transit in vivo was accelerated by TRPV2 agonists or an NO donor. In conclusion, TRPV2 may contribute to intestinal motility through NO production, and TRPV2 is a promising target for controlling intestinal movement.

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Section: Discussionmentioning

confidence: 99%

Involvement of TRPV2 Activation in Intestinal Movement through Nitric Oxide Production in Mice

Mihara¹,

Boudaka²,

Shibasaki³

et al. 2010

J. Neurosci.

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“…There is histological evi dence for the existence o f CCK, VIP, sub stance P, and enkephalins in nerve fibers in the cat pancreas [ 17], If these peptides served a transmitter role, they might mediate some o f the pancreatic response to sham feeding. Such a mechanism has been postulated for the atropine-resistant increase in pancreatic bicarbonate secretion in the pig [18], A prob lem with this hypothesis is that it implies that a completely different set o f efferent neurons is activated by sham feeding versus vagal activation by intestinal stimulants. In ani mals, at least, the intestinal phase o f pan creatic secretion is nearly completely abol ished by atropine [12].…”

Section: Gastric Secretionmentioning

confidence: 99%

Pancreatic Secretory Response to Sham Feeding in Humans

Defilíppí¹,

Solomon²,

Valenzuela³

1982

Digestion

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We studied the pancreatic secretory response to sham feeding alone or during secretin infusion with and without administration of atropine in 10 human subjects. The magnitude of the response to sham feeding was compared to the response to cholecystokinin octapeptide. Sham feeding alone did not significantly increase pancreatic bicarbonate or amylase secretion above basal values. During a background secretin infusion, there was a significant increase of bicarbonate and amylase output (p < 0.05) during sham feeding. The amylase response was approximately 50% of the maximal response to cholecystokinin octapeptide. In the tests with atropine and secretin, sham feeding still caused a significant increment in amylase and bicarbonate output. We conclude that (1) the pancreatic response to sham feeding is not clearly demonstrated without a background of secretin; (2) during secretin infusion sham feeding is a potent stimulant of pancreatic enzyme secretion, and (3) atropine had no significant effect on the pancreatic response to sham feeding under the conditions of this study.

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“…VIP immunoreactivity is present in pancreatic vagal fibres of several species (Larsson & Rehfield, 1979;Bishop, Polak, Green, Bryant & Bloom, 1980) and VIP stimulates a copious serous secretion rich in HCO3-in the pig (Jensen, Fahrenkrug, Holst, Nielsen & Schaffalitzky de Muckadell, 1978). Vagal stimulation results in an increased concentration of VIP in the pancreatic venous effluent, which is reduced concomitantly with the pancreatic secretions on infusion of the inhibitory peptide somatostatin (Fahrenkrug, Schaffalitzky de Muckadell, Holst & Jensen, 1979).…”

Section: Introductionmentioning

confidence: 99%

An investigation into the relative merits of pituitary adenylate cyclase‐activating polypeptide (PACAP‐27) and vasoactive intestinal polypeptide as vagal neuro‐transmitters in exocrine pancreas of rats

Wheeler

Eardley²,

Mcnulty³

et al. 1997

Experimental Physiology

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SUMMARYPancreatic exocrine secretions were collected over 15 min periods and analysed in terms of weight of juice, total HCO3-and total protein in anaesthetized and pithed rats. Pituitary adenylate cyclase-activating polypeptide (PACAP) (i.v.) evoked a serous HCO3-secretion which contained relatively little protein, together with a marked vasodepressor action. The latter was still maximal at lower doses of PACAP, which evoked diminished pancreatic secretions. The effects of PACAP were similar to those evoked by the same dose of VIP and by cervical vagal stimulation, while secretin evoked a much larger secretion of fluid and HCO3-. The time courses of the PACAPevoked secretions were significantly delayed compared with those of VIP. In the pithed rat, PACAP caused the same level of pancreatic secretions as in the anaesthetized rat, though this was now accompanied by a substantial pressor response which was blocked by phentolamine or prazosin, indicating that it was a -adrenoceptor mediated. VIP caused a depressor response in the pithed rat, as well as the same level of pancreatic secretions as in the anaesthetized rat. The putative VIP antagonist [Lys',Pro25,Arg3'4,Tyr6]-VIP (abbreviated as VIPi) caused a selective and significant reduction in the HCO3-secretion evoked by VIP and blocked the vasodepressor response caused by VIP. By contrast, VIPi did not antagonize either the secretory or vasodepressor actions of PACAP. Unilateral electrical stimulation of the cervical vagus nerve evoked significant increases in the weight of juice, total protein and total HC03-secreted. When preceded by injection of VIPi, vagally evoked secretions were unchanged in terms of weight of juice and total protein but had a significantly reduced HCO3 content. These results are consistent with the release of VIP, though not PACAP, as a vagal neurotransmitter in the exocrine pancreas.

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Vasoactive intestinal polypeptide in vagally mediated pancreatic secretion of fluid and HCO3.

Cited by 39 publications

References 14 publications

Involvement of TRPV2 Activation in Intestinal Movement through Nitric Oxide Production in Mice

Involvement of TRPV2 Activation in Intestinal Movement through Nitric Oxide Production in Mice

Pancreatic Secretory Response to Sham Feeding in Humans

An investigation into the relative merits of pituitary adenylate cyclase‐activating polypeptide (PACAP‐27) and vasoactive intestinal polypeptide as vagal neuro‐transmitters in exocrine pancreas of rats

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