Evidence that Somatostatin Releases Endogenous Substance(s) Responsible for Its Presynaptic Inhibitory Effect on Rat Vas deferens and Guinea Pig Ileum

Abstract

The ability of somatostatin to inhibit the muscular twitches elicited by field stimulation of rat vas deferens and guinea pig ileum was studied. Evidence should be summarized which would suggest that the presynaptic inhibitory effect of somatostatin on chemical neurotransmission is indirect. Its effect on vas deferens is partly mediated via α2-adrenoceptors and due to the released noradrenaline, in guinea pig ileum, however, it seems likely that it releases an unidentified inhibitory substance which, in fact, inhibits the release of acetylcholine, and thereby twitches of the ileum. The fast tachyphylaxis seen following repeated administration of the peptide is likely due to its indirect action.

Effects of Schistosoma mansoni infection on somatostatin and somatostatin receptor 2A expression in mouse ileum

“…In normal animals, SOM inhibited the cholinergic neurogenic contractions to EFS. Given the evidence that this inhibitory effect of SOM is indirect, involving presynaptic α 2 adrenoceptors, 18 we further investigated the effect of the α 2 adrenoceptor antagonist yohimbine. However, even in the presence of yohimbine, SOM still inhibited the cholinergic neurogenic contractions to EFS, indicating that adrenergic nerves are not involved in this effect.…”

“…SOM immunoreactivity occurs in a specific subgroup of cholinergic descending interneurones in the myenteric plexus of the small intestine in the guinea‐pig 15,16 and pig, 17 where it has been reported to exert an effect both on the contractile response and on acetylcholine (ACh) release. A previous study 18 of guinea‐pig ileum provided evidence that SOM releases endogenous substances responsible for its presynaptic inhibitory effect. It has been reported that SOM causes the release of noradrenaline (NA) in the guinea‐pig ileum and of a non‐identified substance in the whole ileal wall.…”

Demonstration of the neurotransmitter role of calcitonin gene‐related peptides (CGRP) by immunoblockade with anti‐CGRP monoclonal antibodies

“…Therefore, only one cumulative concentration-response relationship was obtained for CGRP in each tissue. Since tachyphylaxis develops rapidly to somatostatin (Vizi et al, 1984) (Maggi et al, 1993). Individual tissues were exposed to a single concentration of capsaicin.…”

“…Therefore, only one cumulative concentration-response relationship was obtained for CGRP in each tissue. Since tachyphylaxis develops rapidly to somatostatin (Vizi et al, 1984), the response to a single concentration of somatostatin was tested only once in each tissue. Responses to isoprenaline and rat P-endorphin did not desensitize.…”

The putative somatostatin antagonist cyclo-somatostatin has opioid agonist effects in gastrointestinal preparations

“…This substance binds at all somatostatin receptors (see Cycloantagonist SA in Siehler et al, 1999), although some effects of somatostatin may be resistant to CSST inhibition (Shirahase et al, 1993). Of the isolated organs, the guinea-pig ileum is one of the few that show motor responses to somatostatin, namely an inhibition of the cholinergic "twitch" contractions in response to single electrical shocks that are brief enough not to excite smooth muscle cells directly (Guillemin, 1976;Furness and Costa, 1979;Cohen et al, 1979;Jhamandas and Elliott, 1980;Vizi et al, 1984;Feniuk et al, 1995) or partly cholinergic contractions to the neuropeptides neurotensin or caerulein (Monier and Kitabgi, 1981). Although it has been argued that the inhibitory action of somatostatin is indirect (Vizi et al, 1984), it does not seem to involve opioid receptors, as unequivocally shown by all of the above studies that utilized naloxone, an opioid antagonist (Guillemin, 1976;Jhamandas and Elliott, 1980;Monier and Kitabgi, 1981).…”