A somatostatin receptor inhibits noradrenaline release from chick sympathetic neurons through pertussis toxin-sensitive mechanisms: comparison with the action of α2-adrenoceptors
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The role of Cortistatin-14 in the gastrointestinal motility in mice
2018, Pharmacological ReportsCitation Excerpt :However, the mechanisms of CST-14 on GI motility functions is poorly understood. From previous reports, it can be found that there are a close relationship between somatostatin receptor and noradrenaline system [29–32]. For examples, Calhau et al. reported that somatostatin receptor inhibits the release of noradrenaline caused by electrical stimulation of the rat mesenteric artery [30].
Molecular mechanisms underlying the modulation of exocytotic noradrenaline release via presynaptic receptors
2006, Pharmacology and TherapeuticsCitation Excerpt :The simultaneous activation of two such receptors does not cause more inhibition of the Ca2+ channels than the activation of one receptor only (3 in Fig. 4A). This has been investigated in detail for α2-adrenoceptors and somatostatin receptors (Golard & Siegelbaum, 1993): although activation of these two receptors triggered different signaling cascades to inhibit the Ca2+ channels (Boehm et al., 1996a), there was no additivity, neither in the inhibition of Ca2+ currents, nor in the inhibition of noradrenaline release (Boehm & Huck, 1996a). Thus, the signaling cascades of different inhibitory GPCR may converge at the level of voltage-gated Ca2+ channels which are involved in excitation–secretion coupling.
Central suppressive effect of octreotide on the hyperglycemic response to 2-deoxy-D-glucose injection or cold-swim stress in awake rats: Possible mediation role of hypothalamic noradrenergic drive
2001, Brain ResearchCitation Excerpt :Although it is possible that the inhibition of NA re-uptake or the conversion to DHPG may cause the decrease of DHPG following octreotide, several authors have presented evidence that SRIH inhibits the release of NA in in vitro studies. Boehm and Huck have demonstrated that SRIH and seglitide (MK-678, a cyclic hexapeptide SRIH analog) cause an inhibition of electrically evoked tritiated NA release from cultures of chick sympathetic neurons [4]. The affinity of seglitide for SRIH receptors is similar to that of octreotide [13].