Differential action of somatostatin on peptide-induced release of acetylcholine

Kowal, V. O.; Wiley, John W.; Owyang, Chung

doi:10.1152/ajpgi.1989.257.2.g221

Cited by 6 publications

(4 citation statements)

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“…Although it is not well known, one of the suggested mechanisms for the octreotide-induced long QT interval is slowdown of the conducting system due to its inhibitory effects on sinoatrial and atrioventricular nodes via somatostatin receptors [16,17,18,19,20]. The recognition of a long QT interval during octreotide treatment and recovery of the interval after discontinuation led us to suggest that in our case long QT development was secondary to octreotide treatment.…”

Section: Discussionmentioning

confidence: 75%

Octreotide-Induced Long QT Syndrome in a Child with Congenital Hyperinsulinemia and a Novel Missense Mutation (p.Met115Val) in the ABCC8 Gene

Çelik¹,

Cınaz²,

Emeksiz³

et al. 2013

Horm Res Paediatr

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Background/Aims: Congenital hyperinsulinism (CHI) denotes an inappropriate secretion of insulin from pancreatic β-cells in the presence of a low blood glucose level due to various genetic causes. Diazoxide is the first-line medical treatment for CHI. In case of failure, a somatostatin analogue called octreotide is used. A prolonged QT interval is an unusual side effect of octreotide which can be lethal if unrecognized. Case Presentation: We report on a 35-day-old infant who was diagnosed with CHI on the 3rd day of his life and underwent pancreatectomy due to failure of medical treatment at 8 months. His genetic analysis revealed a compound heterozygosity for a novel missense mutation (p.Met115Val) and a nonsense mutation (p.Trp1339X) in the ABCC8 gene. Furthermore, at the 6th month of follow-up, a long QT (0.49 s) was determined by ECG examination, which was normalized following discontinuation of octreotide treatment after pancreatectomy. Thus, the long QT was considered to be secondary to octreotide medication. Conclusion: We recommend ECG monitoring before and during octreotide treatment in order to recognize a prolonged QT interval and to prevent related complications in cases with congenital hyperinsulinemia.

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Section: Discussionmentioning

confidence: 75%

Octreotide-Induced Long QT Syndrome in a Child with Congenital Hyperinsulinemia and a Novel Missense Mutation (p.Met115Val) in the ABCC8 Gene

Çelik¹,

Cınaz²,

Emeksiz³

et al. 2013

Horm Res Paediatr

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“…So, these investigations describe the two main kinds (SOM-positive and Met-enkephalin-positive) of inhibitory neurons, which have distinct neuromodulatory functions in the cholinergic pathways within the ENS. It has also been shown that SOM-induced relaxation of the intestinal muscles is connected with the pre-synaptic inhibition of acetylcholine release by different mechanisms [125,126]. The main mechanism of this SOM activity results from the inhibitory effects on 3’,5’-cyclic adenosine monophosphate [125,126].…”

Section: Functions Of Somatostatin In the Enteric Nervous Systemmentioning

confidence: 99%

“…It has also been shown that SOM-induced relaxation of the intestinal muscles is connected with the pre-synaptic inhibition of acetylcholine release by different mechanisms [125,126]. The main mechanism of this SOM activity results from the inhibitory effects on 3’,5’-cyclic adenosine monophosphate [125,126]. A similar activity of SOM was observed in the submucous plexuses, where in the guinea pig intestine SOM caused the hyperpolarization of about 90% of the total neuronal population [127].…”

Section: Functions Of Somatostatin In the Enteric Nervous Systemmentioning

confidence: 99%

Somatostatin as an Active Substance in the Mammalian Enteric Nervous System

Gonkowski

Rytel

2019

IJMS

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Somatostatin (SOM) is an active substance which most commonly occurs in endocrine cells, as well as in the central and peripheral nervous system. One of the parts of the nervous system where the presence of SOM has been confirmed is the enteric nervous system (ENS), located in the wall of the gastrointestinal (GI) tract. It regulates most of the functions of the stomach and intestine and it is characterized by complex organization and a high degree of independence from the central nervous system. SOM has been described in the ENS of numerous mammal species and its main functions in the GI tract are connected with the inhibition of the intestinal motility and secretory activity. Moreover, SOM participates in sensory and pain stimuli conduction, modulation of the release of other neuronal factors, and regulation of blood flow in the intestinal vessels. This peptide is also involved in the pathological processes in the GI tract and is known as an anti-inflammatory agent. This paper, which focuses primarily on the distribution of SOM in the ENS and extrinsic intestinal innervation in various mammalian species, is a review of studies concerning this issue published from 1973 to the present.

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“…For receptor antagonism experiments, the antagonist was administered followed in 7 min by application of the control dose of agonist in the continued presence of the antagonist. For the experiments with pertussis toxin, the procedure of Kowal et al (14) was used, with incubation of the tissue with pertussis toxin at 200 ng/ml for 3 h. A higher dose of pertussis toxin (1 g/ml) for 3 h was also used. For the experiments with zero calcium, a procedure we have previously used was employed (19), with switching the Krebs solution surrounding the muscle strip to zero calcium with 0.1 mM EGTA for 4 min before the addition of PAF.…”

Section: Methodsmentioning

confidence: 99%

The contractile action of platelet-activating factor on gallbladder smooth muscle

Parkman

James

Ryan

2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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Platelet-activating factor (PAF) may be a mediator of some sequelae of cholecystitis, a disorder with gallbladder motor dysfunction. The aims of this study were to determine the effect and mechanism of PAF on gallbladder muscle. Exogenous administration of PAF-16 or PAF-18 caused dose-dependent contractions of gallbladder muscle strips in vitro with threshold doses of 1 ng/ml and 10 ng/ml, respectively. The PAF-induced contractions were not significantly reduced by TTX, atropine, or hexamethonium but were significantly inhibited with the PAF receptor antagonists ginkolide B and CV-3988. The PAF-induced contraction was reduced by indomethacin. Preventing influx of extracellular calcium with a calcium-free solution nearly abolished the PAF contractile response. Nifedipine inhibited the PAF contractile response, whereas ryanodine had no effect. Pertussis toxin reduced the PAF contractile response. In conclusion, PAF causes gallbladder contraction through specific PAF receptors on gallbladder muscle. These PAF receptors appear to be linked to a prostaglandin-mediated mechanism and to pertussis toxin-sensitive G proteins. The contractile response is largely mediated through the utilization of extracellular calcium influx through voltage-dependent calcium channels.

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Differential action of somatostatin on peptide-induced release of acetylcholine

Cited by 6 publications

References 0 publications

Octreotide-Induced Long QT Syndrome in a Child with Congenital Hyperinsulinemia and a Novel Missense Mutation (p.Met115Val) in the ABCC8 Gene

Octreotide-Induced Long QT Syndrome in a Child with Congenital Hyperinsulinemia and a Novel Missense Mutation (p.Met115Val) in the ABCC8 Gene

Somatostatin as an Active Substance in the Mammalian Enteric Nervous System

The contractile action of platelet-activating factor on gallbladder smooth muscle

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