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)

Remarkable progress has been made during recent years in the central regulation of the hypothalamic releasing and inhibiting factors and the respective anterior pituitary hormones. There are two nearly universal inhibitory organizations: short tuberoinfundibular dopamine (TIDA) neurons and somatostatinergic system originating from the periventricular hypothalamus and terminating to the median eminence. It is now known that e.g. dopamine, noradrenaline and acetylcholine enhance while 5-hydroxytryptamine and GABA inhibit somatostatin secretion. These transmitters are also involved in the regulation of all releasing factors and pituitary hormones. Clinical applications have been developed based on the regulation of prolactin and growth hormone. Inhibitory TIDA neurons are undoubtedly the major determinants of prolactin secretion. Hyperprolactinaemia is one of the most common endocrinological side-effects of the drugs antagonizing dopaminergic transmission. Expectedly, dopaminergic drugs (bromocryptine, lergotrile, piribedil, dopamine and levodopa) are quite effective in reducing high prolactin levels regardless of the reason. The secretion of growth hormone is predominantly under dual dopaminergic control: hypothalamic stimulation and pituitary inhibition. The former masters the function of the normal gland, while the peripheral inhibitory component takes over in acromegalic gland. Hence dopaminergic drugs are able to reduce elevated growth hormone levels in 30-50% of the acromegalic patients. In normal man, dopamine agonists increase growth hormone levels. An analogous situation can be seen in Cushing's disease regarding ACTH secretion.
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PMID:Aminergic regulation of neuroendocrinological functions: theoretical background and some clinical examples. 288 29

The mechanism of somatostatin venoconstriction and tachyphylaxis in the human hand vein in vivo has been investigated. No cross-tachyphylaxis was observed between somatostatin and 5-hydroxytryptamine, noradrenaline, adrenaline, dopamine or tyramine-induced venoconstriction. Somatostatin potentiates the venoconstrictive activity of noradrenaline, adrenaline and dopamine, but not that of 5-hydroxytryptamine and tyramine. Phentolamine antagonizes the somatostatin-induced venoconstriction, whereas methysergide, haloperidol and morphine do not. It is suggested that somatostatin could act on specific receptors in the hand vein, but the mechanism of somatostatin venoconstriction and interaction with vasoactive monoamines remains to be defined.
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PMID:Somatostatin: peripheral venoconstrictive activity and interaction with monoamines in man. 289 Jan 84

1 Intracellular recordings were made from neurones of the submucous plexus and from submucosal arteriolar smooth muscle of guinea-pig ileum for the purpose of examining the the actions of 8-hydroxy-2-(n-dipropylamino)tetralin (8-OH-DPAT). 2 8-OH-DPAT (10 nM-20 microM) had no direct presynaptic or postsynaptic actions on submucous plexus neurones. 3 Membrane hyperpolarizations induced in neurones by noradrenaline or UK 14304 were competitively antagonized by 8-OH-DPAT. For dose-ratios up to 40, Schild plots were linear with slopes not significantly different from unity; pA2 values for the 8-OH-DPAT antagonism of postsynaptic alpha 2-adrenoceptors were 6.9-7.2. 4 The inhibitory synaptic potential, which is due to activation of alpha 2-adrenoceptors located on submucous plexus neurones, was selectively inhibited by 8-OH-DPAT; the IC50 value for inhibition of the inhibitory synaptic potential was 250 nM. 5 Neuronal hyperpolarizations mediated through activation of delta-opioid receptors or somatostatin receptors were unaffected by 8-OH-DPAT (0.1-1 microM). 6 The ability of noradrenaline and UK 14304 to inhibit the release of acetylcholine at synapses in the submucous plexus, and to inhibit the release of the transmitter which mediates the excitatory junction potential in the submucosal arteriolar smooth muscle, was also blocked by 8-OH-DPAT. 7 These results suggest that some of the actions of 8-OH-DPAT previously ascribed to agonism at 5-hydroxytryptamine (5-HT) receptors may actually result from blockade of the actions of endogenously released noradrenaline acting on alpha 2-adrenoceptors.
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PMID:Evidence that 8-hydroxy-2-(n-dipropylamino)tetralin (8-OH-DPAT) is a selective alpha 2-adrenoceptor antagonist on guinea-pig submucous neurones. 289 Mar 93

A 60 year old man developed steatorrhoea, weight loss, mild diabetes mellitus, labile hypertension and limb cramps. Raised plasma concentrations of catecholamines, particularly noradrenaline and a computed tomography-scan showing an adrenal tumour strongly suggested a pheochromocytoma. Adrenoreceptor blockade reversed the symptoms, decreased faecal fat, and increased duodenal trypsin to normal concentrations. After adrenalectomy the patient was asymptomatic and there was no steatorrhoea. The blood glucose concentrations became normal. Immunocytochemistry revealed the tumour cells to store large amounts of enkephalin and somatostatin reactive material and moderate amounts of immunoreactive beta-endorphin and dynorphin.
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PMID:A mixed endocrine adrenal tumour causing steatorrhoea. 289 May 60

The hyperglycemic effects of vertebrate glucagon, octopamine and noradrenaline, are depressed when propranolol or somatostatin is simultaneously injected into emerging adult worker bees. The inhibitory action of the peptidic antagonist (somatostatin) is more marked against the peptidic agonist (glucagon) and the action of the aminergic antagonist (propranolol) is more marked against the aminergic agonist (octopamine). Somatostatin seems to be inactive against the hyperglycemic effects of cyclic AMP itself. Lastly, octopamine and cAMP might share a common stimulatory activity towards the honeybee's hemolymph trehalases.
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PMID:Propranolol and somatostatin interactions with the hyperglycemic effects of glucagon, octopamine, noradrenaline and cAMP in worker honeybees in vivo. 289 82

We have reinvestigated the immunohistochemistry of autonomic axons supplying the guinea-pig uterine artery to determine whether non-noradrenergic paracervical ganglion neurons projecting to the artery contain immunoreactivity to dopamine-beta-hydroxylase (DBH) or somatostatin (SOM) in addition to neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP). In untreated arteries no VIP axons had immunoreactivity to tyrosine hydroxylase (TH), although 9% had immunoreactivity to DBH. Somatostatin immunoreactivity was detected in 25% of non-noradrenergic axons containing NPY and VIP. After in vivo treatment with 6-hydroxydopamine (6-OHDA), noradrenergic axons containing immunoreactivity to NPY, DBH and TH were absent from the adventitia-medial junction. However, 65-70% of the non-noradrenergic axons with NPY and VIP showed DBH immunoreactivity after 6-OHDA. These axons did not show catecholamine fluorescence after incubation with pargyline together with noradrenaline, dopamine or L-DOPA. The number of axons with SOM immunoreactivity increased by 44% after 6-OHDA treatment, but only 24% of SOM axons had DBH immunoreactivity. Surgical destruction of the non-noradrenergic autonomic axons in 6-OHDA-treated animals led to the loss of all DBH immunoreactivity. These results demonstrate that DBH immunoreactivity can be detected in a small proportion of non-noradrenergic axons supplying uterine arteries from untreated animals. After chemical sympathectomy with 6-OHDA, the levels of DBH immunoreactivity in axons of non-noradrenergic neurons increased, and more axons with DBH immunoreactivity were detected. DBH immunoreactivity seemed to increase preferentially in axons with NPY and VIP, but not SOM. The number of NPY, VIP axons containing SOM also increased after 6-OHDA. These findings demonstrate that peripheral neurons containing several different potential neurotransmitters can change their levels of neuropeptides and transmitter-synthesizing enzymes in response to local environmental changes.
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PMID:Increased dopamine-beta-hydroxylase-like immunoreactivity in non-noradrenergic axons supplying the guinea-pig uterine artery after 6-hydroxydopamine treatment. 289 85

1. Electrically evoked contractions of the rat anococcygeus muscle were inhibited in a concentration-dependent manner by somatostatin-14 (SS14), -28 (SS28) and two synthetic hexapeptide analogues: L-363,301 (Pro-Phe-D-Trp-Lys-Thr-Phe) and L-363,586 (N-Me-Ala-Tyr-D-Trp-Lys-Val-Phe), with pIC50 values of 7.41, 7.38, 7.07 and 8.34, respectively. 2. The inhibitory effects of SS14 were dependent on stimulation frequency and external calcium ion concentration. Calcium behaved as a non-competitive antagonist of SS14, it reduced the maximal inhibitory effect of the peptide and at a concentration of 5.08 mM it significantly affected the pIC50 value. 3. SS14 (3 x 10(-7) M) did not affect the tonic actions of bath-applied noradrenaline in the absence of field stimulation. 4. The effects of SS14 persisted in naloxone (10(-5) M) and were, therefore, not due to an action at opiate receptors. Furthermore, experiments involving the lyophilization of bath contents, showed no evidence to support an indirect mechanism involving the release of an endogenous inhibitory substance. 5. High concentrations (10(-5) M) of SS14 or L-363,301 inhibited the relaxation response evoked by electrical stimulation of guanethidine (3 x 10(-4) M)-treated preparations. 6. These results are consistent with similar actions of SS14 on other smooth muscle preparations and are presumed to reflect a presynaptic inhibition of transmitter release by a direct action on somatostatin receptors. The antagonistic effect of calcium on this response is discussed with reference to a possible role in receptor desensitization.
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PMID:The inhibitory effect of somatostatin peptides on the rat anococcygeus muscle in vitro. 290 39

The injection of DL-octopamine to emerging adult honey bees (1 nanomol per individual) promptly rises the haemolymph levels of steroids, diacyl and triacylglycerols (over 100% increase occurring after 10 min). Free fatty acids are then increased (by 131%) 45 mn after injections. These responses are completely abolished by 2.5 nanomol propranolol and 0.07 nanomol cyclic somatostatin. Octopamine thus seems to be more strongly involved in the lipemia than in the glycemia regulation, by contrast with noradrenaline which is, apparently, more active on carbohydrates.
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PMID:[Interaction of propranolol and somatostatin with the octopaminergic response of honeybee lipemia in vivo]. 290 12

We investigated the direct pancreatic effects of noradrenaline in vivo on the secretion of insulin, glucagon, and somatostatin from the in situ pancreas in halothane-anaesthetized dogs. Noradrenaline was infused into the superior pancreatic artery at 12 ng min-1, a rate that did not alter systemic glucose or noradrenaline levels nor heart rate or blood pressure. This pancreatic infusion of noradrenaline did not affect the basal pancreatic output of insulin, yet did markedly inhibit arginine-stimulated insulin secretion. The acute insulin response (AIR) to an intravenous injection of arginine (2.5 g), which was 4293 +/- 1260 microM min-1 under control conditions, was reduced to 1054 +/- 396 microU min-1 by noradrenaline (P less than 0.01). Noradrenaline increased basal pancreatic glucagon output from 321 +/- 130 pg min-1 to 876 +/- 309 pg min-1 after 20 min of infusion (P less than 0.05) and the acute glucagon response (AGR) to arginine, being 1033 +/- 203 pg min-1 under control conditions and 1746 +/- 249 pg min-1 during noradrenaline infusion (P less than 0.05). The basal output of somatostatin did not change during noradrenaline infusion, but arginine-stimulated somatostatin secretion was impaired. The acute somatostatin response (ASLIR) to arginine was 473 +/- 124 fmol min-1 under control conditions and was decreased to 140 +/- 80 fmol min-1 by noradrenaline (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of pancreatic noradrenaline infusion on basal and stimulated islet hormone secretion in the dog. 290 99

In the present study the opioid receptor antagonist properties of the conformationally constrained cyclic octapeptide D-Phe-Cys-Tyr-D-Trp-Lys-Thr-Pen-Thr-NH2 (CTP), which is derived from somatostatin, were investigated, using in vitro functional paradigms of central mu-, delta- and kappa-opioid receptors. Activation of mu-opioid receptors by the enkephalin analogues DADLE or DAGO resulted in a strong inhibition (by 60-70%) of the (electrically evoked) release of [3H]noradrenaline (NA) from superfused cortical slices. This inhibitory effect was antagonized by CTP in a competitive fashion (pA2 value 7.7-7.9). Activation of kappa-opioid receptors by bremazocine selectively inhibited (by 45-50%) the release of [3H]dopamine (DA) from striatal slices, whereas activation of delta-opioid receptors by DADLE caused an inhibition (by 55-60%) of striatal [14C]acetylcholine (ACh) release, but neither of these inhibitory effects was affected by CTP. By itself, CTP inhibited cortical [3H]NA release (by 35-40%), but it did not affect the release of [3H]DA nor that of [14C]ACh from striatal slices. The inhibitory effect of CTP was not antagonized by naloxone. The data indicate that CTP selectively antagonizes mu-opioid receptors, involved in presynaptic inhibition of NA release in the brain. In addition, the peptide by itself causes an inhibition of NA release via a non-opioid receptor-mediated process.
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PMID:Antagonist activity of the cyclic somatostatin analogue CTP at mu- but not delta- and kappa-opioid receptors involved in presynaptic inhibition of neurotransmitter release. 290 79


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