Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Presynaptic receptors in peptidergic neurons within the brain should be considered as an important target upon which different neurotransmitters or neuromodulators can act to affect peptide release. Evidence reviewed in this paper indicates that the median eminence (ME) of the hypothalamus is an area where many such interactions at the presynaptic level take place. Release of LHRH, somatostatin and vasopressin is affected by a variety of neurotransmitters or neuromodulators, such as norepinephrine, dopamine, epinephrine, histamine, cholinergic and opioid agonists, and peptides such as angiotensin II. The actions of these agents were prevented by the use of specific receptor blockers, indicating the specificity of the response evoked. Furthermore, with the use of classical pharmacological approaches, the type and affinity of the receptor involved is well defined. Other agents, such as prostaglandins (PGE2) or steroids (estradiol) were found to affect the activity of the peptidergic neuron at the synaptic terminal by stimulating directly peptide release (as seems to be the case for the PGE2/LHRH interaction) or by changing the sensitivity of the terminal to other transmitters, as shown for estradiol. In conclusion, the evidence presented indicates that the ME is an excellent model to study presynaptic regulation of neural peptide release. A set of criteria was defined within the text to establish the physiological significance of the in vitro studies. Several of the substances tested, and particularly norepinephrine and dopamine, seem to meet all the requirements to be considered physiological presynaptic regulators of neural peptide release at the level of the ME.
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PMID:The median eminence as a model to study presynaptic regulation of neural peptide release. 612 64

A rebound in growth hormone secretion following somatostatin treatment has been shown in several systems where somatostatin suppresses secretion of the hormone. We have developed an in vitro system in which isolated and cultured pituitary cells were perfused after mild trypsinization. After washing, these cells retained their sensitivity and secreted growth hormone (GH) in response to physiological activators (norepinephrine, dopamine, serotonin) or inhibitors (somatostatin) as well as pharmacological activators (PGE2). The variation in GH secretion occurred within a minute after commencement of the infusion and was as rapidly reversible and repeatable minutes later. During somatostatin infusion the GH secretion was not totally suppressed (residual secretion (mean +/- S.D.) 34 +/- 7%). After the infusion a rapid rebound in GH secretion occurred, reaching levels in excess of the pretreatment value of 138 +/- 13%. This rebound effect occurred at doses higher than (10(-10)M) but not at lower doses, even when significant inhibition was observed. The inhibitory effect is of greater magnitude than the rebound effect (rebound = inhibition X 57 +/- 7% (mean +/- S.D.)). Furthermore, rebound was not enhanced by prolongation of somatostatin infusion. These latter results indicate that the rebound in secretion cannot be explained on the sole basis of storage of intracellular GH during somatostatin infusion and in fact suggest the involvement of a process of GH degradation and/or an inhibition of GH synthesis.
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PMID:Differentiation between the somatostatin inhibition and the post-somatostatin rebound observed on growth hormone secretion in vitro. 612 81

Isolated urethral preparations from rabbit and man responded to transmural electrical stimulation with contraction when the basal tension was low, and with relaxation when the preparations were contracted by noradrenaline, clonidine, 5-hydroxytryptamine and lysine vasopressin. Both contractant and relaxant responses were abolished by tetrodotoxin, suggesting that they were caused by the action of transmitters released from nerves. The electrically induced contractions in the rabbit urethra had a threshold frequency of 5 to 6 Hz and maximum was reached at 40 Hz. The responses were markedly reduced by alpha-receptor blockers suggesting that the released contraction-mediating transmitter was mainly noradrenaline. The relaxant response was immediate and rapidly reversible. It was obtained at a threshold frequency of 1 to 2 Hz and maximum was reached at 10 to 15 Hz. It was not inhibited by propranolol, indomethacin, atropine or peptides such as substance P, VIP, vasopressin or somatostatin. Prostaglandin E2, isoprenaline, adenosine-5'-triphosphate and VIP relaxed the noradrenaline contracted rabbit urethra with a time course different from that of the electrically induced relaxation. Nifedipine and "calcium free" solution decreased the noradrenaline induced contraction but did not influence the relaxant response to electrical stimulation. It is suggested that the relaxant response of the isolated noradrenaline-contracted urethra to electrical stimulation is caused by an unknown transmitter released from nerves.
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PMID:Electrically induced relaxation of the noradrenaline contracted isolated urethra from rabbit and man. 613 Nov 47

In isolated rat gastric cells somatostatin and PGE2 were compared in respect to their effects on the cAMP system and on the histamine-stimulated H+-production, measured by 14C-aminopyrine (14C-AP) uptake. Like PGE2 somatostatin activated adenylate cyclase (AC) for all in non-parietal cells. This effect on AC declined in cell fractions with increasing number of parietal cells. Activation of AC or elevation of cellular cAMP and uptake of 14C-AP in response to histamine were inhibited by 10(-9) to 10(-5) mol/1 PGE2 and somatostatin. The results indicate remarkable similarity between somatostatin and PGE2: both activate a non-parietal cell AC and both inhibit H+-production, likely by interfering at the histamine sensitive AC of the parietal cell.
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PMID:Comparison of the effect of PGE2 and somatostatin on histamine stimulated 14C-aminopyrine uptake and cyclic AMP formation in isolated rat gastric mucosal cells. 613 24

Activation of adenylate cyclase (AC) by PGE2, histamine and gastrointestinal hormones was studied in parietal cell-free gastric biopsy specimens from the corpus of patients with proven high gastrin achlorhydria. PGE2, somatostatin, VIP, pentagastrin and secretin activated AC in a concentration-dependent manner both in normal and in atrophic mucosa. Histamine activated AC only in normal gastric mucosa, being entirely ineffective in mucosa devoid of parietal cells. The results indicate that histamine-sensitive AC disappears in patients with achlorhydria, probably due to their loss of parietal cells. Enzyme activity in response to somatostatin, VIP, pentagastrin, secretin and PGE2 remains unchanged in these patients indicating AC localization in nonparietal cells, e.g. chief or mucous cells.
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PMID:Adenylate cyclase in gastric mucosal biopsies from patients with achlorhydria. Stimulation by PGE2, histamine and gastrointestinal hormones. 613 85

The effects of PGE2 and PGD2 on gastric somatostatin and gastrin releases were investigated using the isolated perfused rat stomach. In the presence of 5.5 mM glucose, the infusion of PGE2 elicited a significant augmentation in somatostatin release, but suppressed gastrin secretion from the perfusate. On the other hand, PGD2 did not affect somatostatin release, although the gastrin secretion decreased significantly, the same as after PGE2 infusion. These results suggest that PGE2 and PGD2 may be important in the regulation of gastric endocrine function, but that PGD2 does not affect gastric somatostatin secretion.
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PMID:Effects of prostaglandin E2 and D2 on gastric somatostatin and gastrin secretion. 613 20

Synthetic human pancreatic growth hormone-releasing factor (hpGRF(1-40)-NH2) causes a 100% stimulation of cyclic AMP cell content in rat adenohypophysial cells in culture as early as 1 min after its addition while a maximal 33-fold increase is measured at 40 min. Somatostatin (10 nM) causes a 40-60% inhibition of GRF-induced cyclic AMP accumulation while GH release is inhibited by 90-95% at all time intervals. The inhibitory effect of somatostatin is exerted on the maximal effect of GRF while the ED50 values of GRF action on cyclic AMP cell content (approximately 1 nM) and GH release (approximately 0.1 nM) are not affected by the tetradecapeptide. Prostaglandin E2 causes a 2.5-fold increase in cyclic AMP levels within 1 min after its addition with a maximal 25-fold stimulation measured at 30 min. Although not completely additive, the stimulatory effects of PGE2 and GRF together on cyclic AMP cell content and GH release are more potent than when either substance is present alone. The inhibitory effects of somatostatin on PGE2 action are analogous to those observed in the presence of GRF. The present data suggest that the hypothalamic control of GH secretion by GRF and somatostatin results, at least to a large extent, from the balance between the stimulatory action of GRF and the inhibition of somatostatin on the adenylate cyclase system.
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PMID:Interactions between growth hormone-releasing factor, prostaglandin E2 and somatostatin on cyclic AMP accumulation in rat adenohypophysial cells in culture. 614 Jan 96

The effects of PGE1, PGE2 and PGD2 on somatostatin, insulin and glucagon secretions were investigated at various glucose concentrations using the isolated perfused rat pancreas. At glucose concentrations varying from 0 to 16.7 mM, PGE1 and PGE2 enhanced somatostatin release in a glucose dose-dependent manner. PGE1 did not significantly stimulate insulin secretion at glucose concentrations of 4.4 mM or less, but did at glucose concentrations of 8.8 mM or more, PGE2 augmented insulin release at 4.4 and 16.7 mM glucose, but not in the absence of glucose. Glucagon release was induced by PGE1 and PGE2 in a biphasic pattern with the maximal response in the absence of glucose. Like PGE1 and PGE2, PGD2 stimulated insulin and glucagon release in a glucose-related fashion. PGD2, however, was not capable of stimulating somatostatin release at various glucose concentrations even in the presence of 16.7 mM glucose. In conclusion, PGE1, PGE2, and PGD2 increase insulin and glucagon secretion in a glucose-dependent manner. PGE1 and PGE2 also stimulate somatostatin release, but PGD2 has no effect on somatostatin secretion at the doses studied.
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PMID:Different effects of prostaglandin E1, E2 and D2 on pancreatic somatostatin release. 615 34

The effect of glucagon and its interaction with histamine on adenylate cyclase (AC), cellular cAMP and [14C]aminopyrine ( [14C]AP) uptake, a reliable index of parietal cell H+ production, was studied in isolated rat gastric cells. AC activation in response to glucagon and histamine correlated with the number of parietal cells. Glucagon (10(-10)-10(-6) mol/l) increasingly stimulated AC (maximal effect: 92% by 10(-7) mol/l) and cellular cAMP (86% by 10(-9) mol/l) of fractions enriched with 80% parietal cells but did not cause a pronounced change of the histamine-stimulated enzyme. If there was any interaction, the effect of both hormones was additive. Glucagon neither changed basal [14C]AP uptake nor interfered with that in response to histamine. The data suggest that if glucagon activates a parietal cell AC this process is not followed by parietal cell H+ production. Furthermore, unlike other inhibitors such as somatostatin or PGE2, glucagon does not reduce acid secretion via the cAMP system of the parietal cell.
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PMID:Adenylate cyclase and H+ production of isolated rat parietal cells in response to glucagon and histamine. 632 13

The role of prostaglandins (PGs) in the physiological secretion of the adenohypophyseal hormones, growth hormone (GH) and thyrotropin (TSH), in the unanesthetized, freely behaving male rat was investigated using pharmacological agents. Confirming previous observations, PG synthesis-inhibiting drugs, salicylate and indomethacin (INDO), reduced GH and TSH secretion. Another PG synthesis-inhibiting drug, acetaminophen, also reduced GH and TSH secretion. Antisomatostatin serum administered to INDO-treated rats indicated that somatostatin has a relatively small role in the GH and TSH suppression caused by PG synthesis inhibitors. Stimulation of GH secretion by the alpha 2-adrenergic receptor agonist, clonidine, and by morphine was similar in control and INDO-treated rats whereas PGE2 evoked a significantly greater release of GH in INDO- than in DDC- (dopamine beta-hydroxylase inhibitor-)treated rats. Stimulation of TSH secretion was similar in response to thyrotropin-releasing hormone (TRH) in INDO-treated and control rats and was also similar in response to PGE2 in INDO- and DDC-treated rats. However, clonidine evoked a significantly greater rise in TSH secretion in control than in INDO-treated rats. These results confirm the observation that PGs are important in physiological GH and TSH secretion in the rat and suggest that PGs are involved in GH secretion by interaction proximally to the adrenergic synapse on growth hormone-releasing factor (GRF) neurons and are involved in TSH secretion by interaction postsynaptically to the adrenergic synapse on TRH neurons.
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PMID:Endogenous prostaglandins affect growth hormone and thyrotropin release at a hypothalamic, not a pituitary level. 650 67


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