Somatostatin, release from

In the mouse, whereas no evidence of H3 receptors was found in isolated gastric glands (Muller et al., 1993), in the whole stomach, (R)a-methylhistamine actually increased, and thioperamide decreased acid secretion, thus indicating a definite stimulatory role for H3 receptors in this species (Table 2). Apparently, this excitatory effect, which contrasts with the observations obtained in other models, was due to an inhibitory effect on somatostatin release from fundic D cells (Schubert et al., 1993 Vuyyuru and Schubert 1993). Also, an inhibitory effect on somatostatin secretion mediated by H3 agonists was observed in other species (rat and dog). However, contrarily to what might have been expected, in these species, the inhibitory effect on somatostatin is not followed by an increase in acid secretion, but it is instead followed by a decrease, owing to the predominant H3-mediated inhibition on the release of excitatory mediators (histamine, acetylcholine) from other sites (ECL, cholinergic nerve terminals)... 

Bonanno G, Raiteri M, Emson PC (1988) In vitro release of somatostatin from cerebral cortical slices Characterization of electrically-evoked release. Brain Res 447 92-7 Bonanno G, Gemignani A, Schmid G et al (1996) Human brain somatostatin release from isolated cortical nerve endings and its modulation through GABAb receptors. Br J Pharmacol 118 ... 

Capdevila, ]., Chacos, N., Falck, J.R., Manna, S., Negro-Vilar, A. and Ojeda, S.R. (1983). Novel hypothalamic arachidonate products stimulate somatostatin release from the median eminence. Endocrinology, 113, 421-423... 

Herrmann, J. and R. Bodmeier (1995). The effect of particle microstructure on the somatostatin release from poly(lactide) microspheres prepared by a W/OAV solvent evaporation method. Journal of Controlled Release 36(1-2) 63-71. 

Because somatostatin is so widespread in its distribution, there is some difficulty in assigning an origin for somatostatin released into the circulation. Gastrin and CCK both stimulate somatostatin release from isolated D cells, and this cell type has both CCK, and CCKz receptors. 

Figure 4. Stimulatory pathways of the mammalian parietal cell. The ECL cell is the central endocrine cell releasing histamine for activation of the parietal cell. Its function is regulated centrally by PACAP and galanin and peripherally by gastrin and somatostatin released from G and D cells, respectively.

When the gastritis induced by H. pylori is confined to the antrum, the increase of gastrin and the reduction of somatostatin released by the G and D cells in the antrum, respectively, will increase the drive for acid secretion from the preserved oxyntic mucosa [45]. This increased... 

Figure 4.1. Model of neurogenic inflammation. Stimulation at the skin initiates orthodromic impulses in sensory nerve receptors which elicit antidromic impulses in branching collaterals. The release of neuropeptides such as calcitonin gene-related peptide (CGRP), substance P (SP), and somatostatin (SOM) from nerve terminals ensues and they in turn stimulate the release of histamine (H) and the generation of leukotrienes (LT) from nearby mast cells. These mediators then produce vasodilatation and an increase in vascular permeability. In addition, they act on the nerve terminal to produce further...

The hypothalamic-pituitary-thyroid axis. Acute psychosis or prolonged exposure to cold may activate the axis. Hypothalamic thyroidreleasing hormone (TRH) stimulates pituitary thyroid-stimulating hormone (TSH) release, while somatostatin and dopamine inhibit it. TSH stimulates T4 and T3 synthesis and release from the thyroid, and they in turn inhibit both TRH and TSH synthesis and release. 

Figure 3. Effect of N -methylhistamine produced by Helicobacter pylori on acid secretion On the one hand, this compound may reduce acid secretion by inhibiting, via H3 receptor activation, histamine synthesis and release from ECL cells on the other hand, FI3 receptor activation on D cells, with consequent inhibition of somatostatin release, may increase acid secretion. Additionally, direct activation of H2 receptors on parietal cell by N -metylhistamine must also be considered (this mechanism is not shown in the scheme).

The pancreatic islets consist of four primary cell types alpha (A) cells, which produce glucagon beta (B) cells, which produce insulin delta (D) cells, which produce somatostatin and (F) cells, which produce pancreatic polypeptide. As previously mentioned, this chapter focuses on the functions of insulin and glucagon. The exact physiologic roles of the other pancreatic hormones are not entirely clear. For example, the function of the pancreatic polypeptide released from pancreatic F cells remains to be determined. 

Lewis BM, Dieguez C, Ham J et al. (1989) Effects of glucose on TRH, GHRH, somatostatin and LHRH release from rat hypothalamus in vitro. J Neuroendocrinol 1 437 Lotti G, Delitala G, Devilla L et al. (1977) Reduction of plasma triiodothyronine (T3) induced by propranolol. Clin Endocrinol 6 405... 

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