Vagal regulation of GRP, gastric somatostatin, and gastrin secretion in vitro

1985 ◽  
Vol 248 (4) ◽  
pp. E425-E431 ◽  
Author(s):  
S. Nishi ◽  
Y. Seino ◽  
J. Takemura ◽  
H. Ishida ◽  
M. Seno ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Inhibitory Neuron ◽  
Atropine Sulfate ◽  
Vagus Nerves ◽  
Gastrin Secretion ◽  
Somatostatin Secretion ◽  
Stimulation Of

The effect of electrical stimulation of the vagus nerves on the release of immunoreactive gastrin-releasing peptide (GRP), gastrin, and somatostatin was investigated using the isolated perfused rat stomach. Electrical stimulation (10 Hz, 1 ms duration, 10 V) of the peripheral end of the subdiaphragmatic vagal trunks produced a significant increase in both GRP and gastrin but a decrease in somatostatin. The infusion of atropine sulfate at a concentration of 10(-5) M augmented GRP release and reversed the decrease in somatostatin release in response to vagal stimulation to an increase above basal levels. However, the gastrin response to vagal stimulation was not affected by atropine. The infusion of hexamethonium bromide at a concentration of 10(-4) M significantly suppressed GRP release but did not affect gastrin secretion in response to vagal stimulation. On the other hand, the somatostatin response to vagal stimulation was completely abolished by hexamethonium. These findings lead us to conclude that the intramural GRP neurons might play an important role in the regulation of gastrin as well as somatostatin secretion and that somatostatin secretion may be controlled not only by a cholinergic inhibitory neuron but also by a noncholinergic, e.g., peptidergic stimulatory neuron, both of which may be regulated through preganglionic vagal fibers via nicotinic receptors. In addition, because the infusion of 10(-7) M GRP suppressed the somatostatin secretion, we suggest that either GRP should be excluded from the list of candidates for the noncholinergic stimulatory neurotransmitter for somatostatin secretion or that there are different mechanisms of action for endogenous and exogenous GRP.

Somatostatin restraint of gastrin secretion in pigs revealed by monoclonal antibody immunoneutralization

1992 ◽  
Vol 263 (6) ◽  
pp. G908-G912 ◽  
Author(s):  
J. J. Holst ◽  
P. N. Jorgensen ◽  
T. N. Rasmussen ◽  
P. Schmidt
Keyword(s):  
Monoclonal Antibody ◽  
Electrical Stimulation ◽  
Vagal Stimulation ◽  
Binding Capacity ◽  
Functional Coupling ◽  
Vagus Nerves ◽  
Basal Secretion ◽  
Gastrin Cells ◽  
Gastrin Secretion ◽  
Stimulation Of

We studied the functional coupling between antral somatostatin and gastrin cells in isolated perfused porcine antrum using immunoneutralization with monoclonal antibodies against somatostatin. Their binding affinity was 10(11) l/mol, and the final binding capacity was 11.7 nmol/ml. Antibody infusion within 1 min increased gastrin secretion, reaching a rate of 349 +/- 64% (means +/- SE, n = 7) of basal secretion (59 +/- 5 pmol/l) after 5 min. The effect of somatostatin at 10(-9) mol/l, which inhibited gastrin secretion from 58 +/- 11 to 14 +/- 3 pmol/min (n = 4), was abolished by antibody infusion. Electrical stimulation of the vagus nerves (n = 7) performed during antibody infusion increased gastrin secretion from 224 +/- 61 to 328 +/- 55 pmol/min, not significantly different from the increase in control experiments from 43 +/- 9 to 118 +/- 20 pmol/min, indicating that the vagal stimulation of gastrin secretion does not depend on mechanisms involving somatostatin. We conclude that paracrine antral somatostatin secretion is one of the most important factors regulating basal gastrin secretion in pigs.

Electrophysiological identification of vagally innervated enteric neurons in guinea pig stomach

1992 ◽  
Vol 263 (5) ◽  
pp. G709-G718 ◽  
Author(s):  
M. Schemann ◽  
D. Grundy
Keyword(s):  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Enteric Neurons ◽  
Command Neurons ◽  
Myenteric Neurons ◽  
Release Of Acetylcholine ◽  
Vagal Innervation ◽  
Guinea Pig Stomach ◽  
Stimulation Of

Myenteric "command neurons" are thought to be the interface between extrinsic and intrinsic controls of gut functions and are thought to be responsible for transmission of vagal impulses to enteric microcircuits. To identify, electrophysiologically, myenteric neurons responding to electrical stimulation of the vagus, we developed an in vitro preparation of the gastric myenteric plexus in which the vagal innervation was preserved. The majority of myenteric neurons [102 of 155 (66%)] received fast excitatory postsynaptic potentials (fEPSPs) after stimulation of the vagus. The proportion of neurons receiving vagal input was highest at the lesser curve (98%) and decreased gradually when recordings were made from neurons located toward the greater curve. Only a small proportion of neurons (4 of 85 cells) showed a slow EPSP after a burst of vagal stimulation. No postsynaptic inhibitory potentials were observed. There was no preferential vagal input to either gastric I, gastric II, or gastric III neurons. The fEPSPs were due to the release of acetylcholine acting postsynaptically on nicotinic receptors. The behavior of the fEPSPs suggests multiple vagal inputs to a majority of myenteric neurons. Our observations call into question the concept of enteric command neurons in favor of a divergent vagal input with widespread modulatory influences over gastric enteric neurotransmission.

scholarly journals Effect of Electrical Stimulation of the Vagus Nerves on Bile Secretion in Anaesthetized Sheep

1976 ◽  
Vol 29 (4) ◽  
pp. 351 ◽  
Author(s):  
MichaeI Pass ◽  
Trevor Heath
Keyword(s):  
Electrical Stimulation ◽  
Bile Salt ◽  
Maximum Rate ◽  
Vagal Stimulation ◽  
Bile Secretion ◽  
Vagus Nerves ◽  
Bile Formation ◽  
Vagal Innervation ◽  
Bicarbonate Output ◽  
Stimulation Of

Bile was collected before and during electrical stimulation of the vagus nerves in acute experiments on sheep with ligated cystic ducts. Most stimuli caused no change in: bile formation, but a 10-V, 10-Hz stimulus caused a slight increase in bicarbonate output. Neither the response to infused secretin nor the maximum rate of bile salt transpoit by liver cells changed during vagal stimulation; It was concluded that the vagal innervation of the liver is not likely to playa major role in the regulation of bile formation in sheep.

NO mediates gastric relaxation after brief vagal stimulation in anesthetized dogs

1995 ◽  
Vol 269 (2) ◽  
pp. G255-G261 ◽  
Author(s):  
A. L. Meulemans ◽  
J. G. Eelen ◽  
J. A. Schuurkes
Keyword(s):  
Electrical Stimulation ◽  
Vagal Stimulation ◽  
Gastric Volume ◽  
Maximal Effect ◽  
Platinum Electrodes ◽  
Frequency Dependent ◽  
Vagal Nerves ◽  
Guinea Pig Stomach ◽  
Stimulation Of

In vitro studies showed that relaxations induced after vagal stimulation of the guinea pig stomach are mediated via nitric oxide (NO). The role of NO in canine gastric relaxation in response to vagal stimulation has as yet not been studied. The present study examined the influence of NG-nitro-L-arginine (L-NNA) on gastric relaxations after vagal nerve stimulation in the anesthetized dog. In beagle dogs (n = 7), the ventral and dorsal abdominal vagal nerves were connected to a pair of platinum electrodes. Gastric tone was measured by means of a barostat. Changes in gastric motility were measured with force transducers sutured on the fundus and the antrum. The cervical vagi were sectioned, and dogs were given atropine (0.2 mg/kg i.v.) and guanethidine (5 mg/kg i.v.). Electrical stimulation of the vagal trunks (19 V, 1-ms duration, for 15 s every 2 min, 1-30 Hz) induced frequency-dependent increases in volume. On the fundus, frequency-dependent relaxations could be observed (maximal effect at 5 mmHg and at 10 Hz). During electrical stimulation, the spontaneous antral contractions were completely blocked. After cessation of the stimulus, "rebound" contractions could be observed. L-NNA (5 mg/kg i.v.) completely blocked the increases in gastric volume and the relaxations on the fundus. On the antrum, however, contractions were observed during the electrical stimulation. L-Arginine (250 mg/kg i.v.) gradually restored the relaxations on electrical stimulation. This study demonstrates that NO mediates short-lasting vagally induced gastric relaxations in the anesthetized dog.

GRP-producing nerves control antral somatostatin and gastrin secretion in pigs

1987 ◽  
Vol 253 (6) ◽  
pp. G767-G774 ◽  
Author(s):  
J. J. Holst ◽  
S. Knuhtsen ◽  
C. Orskov ◽  
T. Skak-Nielsen ◽  
S. S. Poulsen ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Substance P ◽  
Nerve Fibers ◽  
Antral Mucosa ◽  
Nerve Supply ◽  
Vagus Nerves ◽  
Vagus Stimulation ◽  
Gastrin Secretion ◽  
Stimulation Of

By immunohistochemistry, nerve fibers containing gastrin-releasing polypeptide (GRP)-like immunoreactivity were identified close to the somatostatin (SS)-producing cells of the gastric antral mucosa. We, therefore, studied the possible role of GRP in the control of antral SS secretion by use of isolated perfused pig antrum with intact vagus nerve supply. Electrical stimulation of the vagus nerves at 4 Hz increased the antral release of GRP up to 10-fold and increased SS output 2- to 3-fold. Atropine at 10(-6) M had no effect on these responses. Intra-arterial GRP increased SS secretion significantly at 10(-10) M and eightfold at 10(-8) M, whereas gastrin secretion was stimulated significantly at 10(-11) M and maximally at 10(-10) M and inhibited at 10(-8) M. Preperfusion with a GRP antagonist ([D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P) or Fab fragments of antibodies against GRP abolished the effects of vagus stimulation on gastrin and somatostatin output. Gastrin in concentrations up to 10(-7) M was without effect on SS secretion. We conclude that electrical stimulation of the vagus nerves increases antral SS gastrin secretion and that GRP is a likely transmitter.

Interaction of serotonin with vagal- and ACh-induced bronchoconstriction in canine lungs

1982 ◽  
Vol 52 (4) ◽  
pp. 964-966 ◽  
Author(s):  
J. R. Sheller ◽  
M. J. Holtzman ◽  
B. E. Skoogh ◽  
J. A. Nadel
Keyword(s):  
Electrical Stimulation ◽  
Nerve Terminal ◽  
Vagal Stimulation ◽  
Vagus Nerves ◽  
Parasympathetic Ganglia ◽  
Anesthetized Dogs ◽  
Postganglionic Nerve ◽  
Stimulation Of

The bronchoconstrictor response to electrical stimulation of the peripheral ends of both cut cervical vagus nerves was potentiated by serotonin aerosols in 10 experiments in 7 anesthetized dogs. The bronchoconstrictor response to acetylcholine (ACh) aerosols was unchanged after serotonin. We conclude that serotonin acts at the level of the parasympathetic ganglia or the postganglionic nerve terminal to potentiate the bronchoconstrictor response to vagal stimulation.

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

1979 ◽  
Vol 237 (6) ◽  
pp. E535 ◽  
Author(s):  
J Fahrenkrug ◽  
O B Schaffalitzky de Muckadell ◽  
J J Holst ◽  
S L Jensen
Keyword(s):  
Electrical Stimulation ◽  
Vasoactive Intestinal Polypeptide ◽  
Pancreatic Secretion ◽  
Vagal Stimulation ◽  
Porcine Pancreas ◽  
Pancreatic Fluid ◽  
Stimulation Of ◽  
Intestinal Polypeptide

The role of nerves that liberate vasoactive intestinal polypeptide (VIP) in the porcine pancrease as mediators of the atropine-resistant action of the vagus on flow and bicarbonate (HCO3) secretion was examined. Efferent electrical stimulation of the vagus in atropinized pigs produced a profuse flow of pancreatic juice with high HCO3 content concomitantly with a significant increase in pancreatic VIP output from 13 to 113 fmol/min. Intravenous administration of somatostatin (SRIF) during continuous electrical vagal stimulation caused a parallel suppression of the VIP release and the pancreatic fluid and HCO3 secretion to prestimulatory values. The SRIF-induced reduction in fluid and HCO3 secretion seemed to be mediated via an inhibition of the VIP release rather than through a direct effect on the exocrine cells, inasmuch as SRIF did not influence the VIP-provoked exocrine response from the in vitro isolated perfused porcine pancreas. The results support the view that VIP is transmitter in the vagally induced atropine-resistant water and HCO3 secretion from the porcine pancreas.

Regulation of gastrin and somatostatin secretion by cholinergic and noncholinergic intramural neurons

1982 ◽  
Vol 243 (6) ◽  
pp. G442-G447 ◽  
Author(s):  
M. L. Schubert ◽  
K. N. Bitar ◽  
G. M. Makhlouf
Keyword(s):  
Electrical Stimulation ◽  
Cholinergic Neuron ◽  
Maximal Response ◽  
Rat Stomach ◽  
Gastrin Secretion ◽  
Somatostatin Secretion ◽  
Stimulation Of

The regulation of gastrin and somatostatin secretion by intramural neurons was examined in the isolated vascularly perfused rat stomach. The optimal modalities of transmural electrical stimulation of the antrum were established to be 40 V and 10 Hz. Stimulation at increasing cycle durations (0.1-4 ms) caused increasing gastrin secretion that was progressively more resistant to atropine. The maximal gastrin response to 4-ms cycles was equal to the maximal response to methacholine. However, the response to methacholine was inhibited 70-90% by atropine, whereas the response to 4-ms cycles was inhibited by 15% only. Stimulation at all cycle durations caused a decrease in somatostatin secretion. Atropine converted the decrease to an increase, from which it was concluded that before atropine somatostatin secretion was the net result of cholinergic inhibition and noncholinergic stimulation of somatostatin. The results indicate that cholinergic and noncholinergic intramural neurons are predominantly but not exclusively activated by 0.1- and 4-ms cycles, respectively. The existence of distinct neurons was supported by results of stimulation of preganglionic vagal fibers with 0.2- and 4-ms cycles. The findings are consistent with a model according to which gastrin secretion is regulated by two interdependent intramural neurons: a cholinergic neuron that stimulates gastrin secretion indirectly by inhibition of somatostatin secretion and a noncholinergic neuron that stimulates gastrin secretion directly by release of a peptide stimulant, probably bombesin.

scholarly journals Establishment of a New Device for Electrical Stimulation of Non-Degenerative Cartilage Cells In Vitro

2021 ◽  
Vol 22 (1) ◽  
pp. 394
Author(s):  
Simone Krueger ◽  
Alexander Riess ◽  
Anika Jonitz-Heincke ◽  
Alina Weizel ◽  
Anika Seyfarth ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Electric Fields ◽  
Cartilage Tissue ◽  
Type I ◽  
Dependent Manner ◽  
New Device ◽  
Alternating Electric Fields ◽  
Cartilage Cells ◽  
Stimulation Of

In cell-based therapies for cartilage lesions, the main problem is still the formation of fibrous cartilage, caused by underlying de-differentiation processes ex vivo. Biophysical stimulation is a promising approach to optimize cell-based procedures and to adapt them more closely to physiological conditions. The occurrence of mechano-electrical transduction phenomena within cartilage tissue is physiological and based on streaming and diffusion potentials. The application of exogenous electric fields can be used to mimic endogenous fields and, thus, support the differentiation of chondrocytes in vitro. For this purpose, we have developed a new device for electrical stimulation of chondrocytes, which operates on the basis of capacitive coupling of alternating electric fields. The reusable and sterilizable stimulation device allows the simultaneous use of 12 cavities with independently applicable fields using only one main supply. The first parameter settings for the stimulation of human non-degenerative chondrocytes, seeded on collagen type I elastin-based scaffolds, were derived from numerical electric field simulations. Our first results suggest that applied alternating electric fields induce chondrogenic re-differentiation at the gene and especially at the protein level of human de-differentiated chondrocytes in a frequency-dependent manner. In future studies, further parameter optimizations will be performed to improve the differentiation capacity of human cartilage cells.

Vagal stimulation-induced gastric damage in rats

1991 ◽  
Vol 261 (1) ◽  
pp. G104-G110
Author(s):  
L. E. Hierlihy ◽  
J. L. Wallace ◽  
A. V. Ferguson
Keyword(s):  
Vagal Stimulation ◽  
Mucosal Damage ◽  
Vagal Afferents ◽  
Gastric Damage ◽  
Gastric Mucosal Damage ◽  
Sprague Dawley ◽  
Vagus Nerves ◽  
Sprague Dawley Rats ◽  
Series Of Experiments ◽  
Stimulation Of

The role of the vagus nerve in the development of gastric mucosal damage was examined in urethan-anesthetized male Sprague-Dawley rats. Electrical stimulation was applied to the vagus nerves for a period of 60 min, after which macroscopic gastric damage was scored and samples of the stomach were fixed for later histological assessment. Damage scores were assigned blindly based on a 0 (normal) to 3 (severe) scale. Stimulation of vagal afferents or efferents in isolation did not result in significant damage to the gastric mucosa (P greater than 0.1). In contrast, stimulation of both intact vagus nerves resulted in significant gastric mucosal damage (mean damage score, 2.0 +/- 0.33, P less than 0.01). A second series of experiments demonstrated this gastric damage to be induced within 30-60 min; extending the stimulation period to 120 min did not worsen the gastric damage scores significantly (P greater than 0.1). In a third study, stimulation of both intact vagus nerves after paraventricular nucleus (PVN) lesion resulted in damage scores (0.33 +/- 0.17) that were significantly reduced compared with intact PVN and non-PVN-lesioned animals (P less than 0.01). These results indicate that the development of vagal stimulation-induced gastric damage requires the activation of both afferent and efferent vagal components and suggest further that such damage is dependent upon an intact PVN.

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