Elsevier

Peptides

Volume 4, Issue 1, January–February 1983, Pages 49-53
Peptides

Modulation of cholinergic neurotrasmitter release from myenteric plexus by somatostatin

https://doi.org/10.1016/0196-9781(83)90164-XGet rights and content

Abstract

Efflux of radiolabeled acetylcholine (Ach) was studied in vitro using myenteric plexus-longitudinal muscle strips from guinea pig small intestine. The data showed that somatostatin (6.0×10−7 M) depressed resting output of Ach from enteric neurons and this inhibition was unaltered in the presence of naloxone (1.0×10−6 M). The inhibition by somatostatin on field-stimulated Ach release was dose-dependent but this inhibition was never complete; there was a 40% fraction of total release remained resistant to somatostatin. Both caerulein (2.85×10−9 M) and guanidine (3.0×10−3 M) stimulated release of [H3]-Ach from plexus neurons. The release of Ach induced by guanidine or caerulein was also susceptible to inhibition by somatostatin (6.0×10−7 M). This study provides functional evidence to further substantiate an inhibitory action on plexus cholinergic neurons by somatostatin.

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  • The role of somatostatin and its receptors (sstr2, sstr5) in the contractility of gilt inflamed uterus

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    SOM could regulate uterine contractility also indirectly by effect on the production and release of substances involved in this organ contriction. Exist data showing inhibitory effect of SOM on ACh release from intestine myenteric neurons (Yau et al., 1983) and, as it was mentioned above, the ability of SOM to stimulate the production of PGE2 in neonatal rat gial cells (Dror et al., 2008) and LTC4 release from human skin mast cells (Benyon et al., 1989). Earlier studies revealed that ACh (Jana et al., 2019) and PGF2α, PGE2, PGI2, LTC4 and LTD4 (Kucharski et al., 2007; Jana et al., 2010; Jana et al., 2013; Jana et al., 2015), affect the contractility of the healthy and inflamed porcine uterus.

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