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)

Somatostatin in concentrations of 10(-6) to 10(-8) M inhibited basal release of thyrotropin releasing factor in organ culture of rat hypothalamus. Norepinephrine in doses of 10(-4)--10(-6) M induced release of thyrotropin releasing factor which increased progressively with time and was temperature and dose dependent. This enhanced thyrotropin-releasing-factor release was inhibited by somatostatin at 10(-6)--10(-8) M.
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PMID:Somatostatin inhibits release of thyrotropin releasing factor from organ cultures of rat hypothalamus. 10 Jul 86

The rate of insulin, glucagon, and somatostatin secretion was measured from isolated rat islets maintained in a perifusion system. The effect of norepinephrine (NE) was simultaneously determined on the release rate of all three hormones. Norepinephrine was employed at an acute dose of 10 micrometers and in graded doses from 1 nM to 10 micrometers in the presence of high (22 mM) and low (1.4 mM) glucose conditions, insulin secretion was maximally inhibited at 10 micrometers NE concentration and was significantly depressed at 100 mM NE concentration. Under both high and low glucose conditions, glucagon release was maximally stimulated at 10 micrometers NE concentration and was significantly elevated at 10 nM NE concentration. Under high and low glucose conditions, somatostatin release was inhibited by 10 micrometers NE concentration and was significantly depressed at 100 nM NE concentration. During the initial maximal stimulation of glucagon, NE inhibition of somatostatin and insulin was prevented, possibly by the high level of glucagon released. A paracrine effect of glucagon on beta and delta cells is proposed.
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PMID:Effect of norepinephrine on insulin, glucagon, and somatostatin secretion in isolated perifused rat islets. 38 55

1. Unitary potassium currents were recorded in outside-out patches of membrane from guinea-pig submucosal neurones. The actions of alpha 2-adrenoceptor agonists, somatostatin and [Met5]enkephalin were studied. 2. Three main groups of background potassium channels were active. At -70 mV with 160 mM-potassium on both sides of the membrane, they had conductances of 30-65 (small), 120-160 (intermediate) and 220-260 pS (large). 3. The open channel current-voltage relation showed only constant-field rectification. Extracellular barium (2 mM) and caesium (2 mM) decreased inward but not outward currents. Tetraethylammonium (10 mM) had no effect. 4. Noradrenaline, somatostatin and [Met5]enkephalin each increased the open probability of all three classes of channel when two or more unitary amplitude channels were active in the membrane patch. Agonists were ineffective when no channel, or a single channel, was discernible in the patch. Agonists did not cause the appearance of unitary currents distinct from those seen prior to their application. 5. The effect of the agonists required intracellular guanosine 5'-triphosphate. 6. The results show that the hyperpolarization of submucosal plexus neurones by noradrenaline, somatostatin and [Met5]enkephalin results from the increased opening of at least three types of background potassium channel, and that the coupling from the receptors to the channels is maintained in excised membrane patches.
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PMID:Potassium channels opened by noradrenaline and other transmitters in excised membrane patches of guinea-pig submucosal neurones. 135 59

The pineal contains a large number of classical transmitters and neuropeptides. Some of these neurochemicals are involved in the regulation of serotonin N-acetyltransferase (NAT) activity and hence in melatonin synthesis. Synaptic ribbons present in the pineal gland also exhibit a numerical day/night rhythm parallel to that of NAT activity. There is scarcity of information regarding the regulation of synaptic ribbon (SR) numbers. In the present study, we have investigated in vitro effects of a number of classical neurotransmitters and neuropeptides. NAT activity was used to monitor melatonin synthesis under the experimental conditions used. Norepinephrine (NE), Delta sleep-inducing peptide (DSIP), vasoactive intestinal polypeptide (VIP), adenosine and N-acetyl-asp-glu (NAAG) significantly increased NAT activity in rat pineal. DSIP and VIP also increase the stimulatory effect of NE on NAT activity. These neurochemicals had no effect on SR numbers. Gamma aminobutyric acid (GABA), serotonin and taurine affected neither NAT activity nor SR. Somatostatin increased SR numbers significantly, without having any effect on NAT activity. The effect of somatostatin is regarded to be pharmacologic, since rather high dosages (10(-4) M) were required to obtain a significant effect. Although somatostatin is present in the pineal and may change rhythmically, the inconsistency of the day/night rhythmicity and the lack of such a rhythm in female rats and male gerbils speaks against an important physiological role of somatostatin in regulating SR numbers.
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PMID:In vitro effects of putative neurotransmitters on synaptic ribbon numbers and N-acetyltransferase activity in the rat pineal gland. 135 54

1. Whole-cell recordings were made from submucosal neurones acutely dissociated from guinea-pigs. The actions of noradrenaline, somatostatin and [Met5]enkephalin on currents carried by calcium ions were studied. 2. On depolarization from a holding potential of -70 mV, an inward current activated at -40 mV, reached its peak amplitude at 10 mV and reversed to outward at 72 mV (with external calcium of 5 mM and internal caesium of 160 mM). 3. Cadmium, nickel and cobalt reversibly blocked the calcium current; concentrations causing 50% block were 2.5, 500 and 2000 microM respectively. The calcium current (holding at -70 or -30 mV) was reversibly blocked by omega-conotoxin (100 nM), and unaffected by Bay K 8644 (0.1-10 microM) and nifedipine (1 microM). Cadmium caused an outward shift in holding current at -30 mV, implying that there was a persistent inward calcium current at this potential. 4. Noradrenaline, somatostatin and [Met5]enkephalin decreased the calcium current. The maximal inhibition observed with any one agonist, or with a combination of two agonists, did not exceed 50%; concentrations giving half-maximal inhibition were 5.5 microM for noradrenaline, 4 nM for somatostatin and 1 microM for [Met5]enkephalin. The inhibition was independent of membrane potential. All three agonists also reduced the persistent calcium current at -30 mV. 5. Inhibition of the calcium current by noradrenaline occurred with a latency of not less than 175 ms; cadmium applied by the same method depressed the current within 5-45 ms. 6. Experiments with selective agonists and antagonists indicated that the receptor types involved in calcium current inhibition were alpha 2-adrenoceptors and delta-opioid receptors. Somatostatin acted at a distinct receptor. 7. Calcium currents were also inhibited by intracellular dialysis with guanosine 5'-O-(3-thiotriphosphate) (GTP-gamma-S). Agonists were ineffective in cells pre-treated with pertussis toxin, but their action was restored when purified GTP-binding proteins (Go or Gi) were included in the intracellular recording solution. 8. It is concluded that noradrenaline, somatostatin and [Met5]enkephalin act at their respective receptors on guinea-pig submucosal neurones to inhibit a voltage-dependent calcium current. Activation of the same receptors also increases a potassium conductance in these cells: in both cases a pertussis-sensitive G protein is involved.
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PMID:Inhibition of calcium currents by noradrenaline, somatostatin and opioids in guinea-pig submucosal neurones. 198 21

1. Intracellular recordings were made from submucosal neurones of the guinea-pig ileum. The actions of noradrenaline, somatostatin and [Met5]enkephalin on nicotinic synaptic potentials (EPSPs) were studied. 2. In one series of experiments, agonists were applied by superfusion; noradrenaline (0.1-20 microM) decreased EPSP amplitude by 95-100% in all neurones. Similar application of somatostatin (1-100 nM) inhibited EPSPs in about half the neurones by a maximum of 40%. [Met5]enkephalin (0.1-10 microM) did not alter EPSPs. Idazoxan and yohimbine competitively antagonized the action of noradrenaline with dissociation equilibrium constants of 20 and 30 nM respectively. 3. In another series of experiments, noradrenaline and somatostatin were applied locally from a pipette so that they reached presynaptic terminals but not the cell bodies or axons of the presynaptic cell: noradrenaline inhibited EPSPs by 90% in all neurones but somatostatin had no effect. When applied locally to the cell bodies giving rise to the presynaptic fibres, both agonists inhibited EPSPs in half the neurones by 40%. 4. When noradrenaline was applied locally to presynaptic terminals, the latency to onset of noradrenaline to inhibit EPSPs was 45-160 ms; cadmium applied similarly depressed EPSPs in 5-50 ms. 5. Pertussis toxin pre-treatment only partially blocked presynaptic inhibition caused by noradrenaline but abolished the reduction of EPSP amplitude by somatostatin. 6. It is concluded that noradrenaline and somatostatin reduce the amplitude of the fast EPSP because they hyperpolarize cell bodies and prevent action potential initiation. Noradrenaline, but not somatostatin, has an additional action to inhibit acetylcholine release by acting at nerve terminal receptors. 7. The presynaptic inhibitory action of noradrenaline results from activation of alpha 2-adrenoceptors at nerve terminals but the mechanism(s) by which these presynaptic receptors act cannot be explained adequately by either activation of a potassium conductance and/or inhibition of a calcium conductance.
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PMID:Mechanisms underlying presynaptic inhibition through alpha 2-adrenoceptors in guinea-pig submucosal neurones. 198 22

The dog pituitary pars intermedia (PI) appears to consist of relative large numbers of ACTH-containing cells in addition to the more abundant alpha MSH-containing cells. Since regulation of PI secretion probably varies across mammalian species, this study was undertaken to identify substances potentially involved in the control of dog PI POMC peptide secretion and to determine if these substances altered the secretion of immunoreactive (IR) ACTH and IR-alpha MSH in a parallel fashion. Pituitary neurointermediate lobes from dogs were collected and dispersed, and the PI cells obtained were perifused. For comparison, rat PI and pars distalis (PD) cells as well as dog PD cells were similarly collected and perifused. Dog PI cells secreted IR-alpha MSH at a basal rate of 125 +/- 59 (mean +/- SD) pg/min.10(5) cells and IR-ACTH at a rate of 40 +/- 9 pg/min.10(5) cells (molar IR-alpha MSH/IR-ACTH = 10). In contrast, secretion rates for IR-alpha MSH and IR-ACTH from perifused rat PI cells were 171 +/- 108 and 3 +/- 2 pg/min.10(5) cells, respectively (molar IR-alpha MSH/IR-ACTH = 179). Using Sephadex G-50 gel filtration chromatography, virtually all of the IR-beta-endorphin secreted by dog PI cells eluted near beta-endorphin (1-31). In addition, all of the IR-alpha MSH secreted by dog PI cells coeluted with synthetic alpha MSH on the G-50 column, but IR-ACTH appeared in two peaks, one eluting near porcine ACTH-(1-39) and another, apparently larger mol wt species. Dopamine and somatostatin were found to inhibit the secretion of IR-alpha MSH and IR-ACTH from perifused dog PI cells in a parallel and dose-dependent fashion. Norepinephrine and epinephrine similarly inhibited POMC peptide secretion, but this effect was blocked by haloperidol, suggesting that it was mediated through a dopamine receptor. CRF stimulated the secretion of both hormones from dog PI, and this effect was abolished by treatment of the cells with either dopamine or somatostatin. Cortisol had no effect on either basal or CRF-stimulated secretion of IR-alpha MSH or IR-ACTH from dog PI cells, but it did inhibit CRF-stimulated IR-ACTH from perifused dog PD. These results suggest that 1) dog PI secretes considerably more IR-ACTH than that in the rat; 2) the probable separate cell sources of IR-alpha MSH and IR-ACTH in dog PI are regulated in an identical fashion; and 3) dopamine, somatostatin, and CRF may function in the physiological or pathophysiological regulation of dog PI.
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PMID:Regulation and secretion of proopiomelanocortin peptides from isolated perifused dog pituitary pars intermedia cells. 253 71

The substances stimulating the release of immunoreactive corticotropin-releasing factor from cultured human placental cells were investigated. Monolayer primary cultures of trophoblast cells from pregnant women at term were used. The immunoreactive corticotropin-releasing factor released in the culture medium eluted from high-performance liquid chromatography with the same retention time as human corticotropin-releasing factor. Norepinephrine and acetylcholine increased immunoreactive corticotropin-releasing factor release into the culture medium in a dose-related manner. Epinephrine was partially active, whereas dopamine and serotonin did not induce significant changes of immunoreactive corticotropin-releasing factor release from placental cultures. Angiotensin II, interleukin-1, oxytocin, and arginine-vasopressin also increased placental immunoreactive corticotropin-releasing factor release in a dose-related manner, whereas other peptides (vasoactive intestinal peptide, substance P, somatostatin, atrial natriuretic factor, interleukin-2) were ineffective. These results showed that several neurotransmitters and peptides stimulate the release of immunoreactive corticotropin-releasing factor from placental cells, suggesting their possible involvement in the physiologic regulation of placental immunoreactive corticotropin-releasing factor release during pregnancy and parturition.
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PMID:Neurotransmitters and peptides modulate the release of immunoreactive corticotropin-releasing factor from cultured human placental cells. 256 97

The effect of plasma noradrenaline concentrations within the physiological range (less than 5-6 nM) on the endocrine pancreas was investigated in 9 nondiabetic volunteers. Noradrenaline significantly inhibited plasma insulin levels but did not change plasma glucagon and somatostatin concentrations.
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PMID:Effects of physiological increases in plasma noradrenaline on the human endocrine pancreas. 257 94

We compared the effects of electrical stimulation of the splanchnic nerves and infusions of neuropeptide Y, noradrenaline or a combination of the two on pancreatic vascular resistance and exocrine and endocrine secretion. For these studies we used isolated perfused pig pancreas with preserved splanchnic nerve supply. The exocrine secretion was stimulated with physiological concentrations of secretin and cholecystokinin octapeptide. Noradrenaline and NPY at 10(-8) M both increased pancreatic perfusion pressure. Their effects were additive and similar in magnitude to that of electrical stimulation of the splanchnic nerves at 4-8 Hz. Nerve stimulation as well as NPY and noradrenaline infusions inhibited exocrine secretion, but an additive effect could not be demonstrated. Neither NPY nor noradrenaline could reproduce the stimulatory effect of nerve stimulation on glucagon secretion, nor the weak inhibitory effect on somatostatin secretion. NPY alone had no effect on insulin secretion and did not influence the inhibitory effect of noradrenaline. It is concluded that NPY is likely to cooperate with noradrenaline in the control of pancreatic blood flow, whereas its role in the control of pancreatic secretion is likely to be of minor importance, if any.
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PMID:On the regulatory functions of neuropeptide Y (NPY) with respect to vascular resistance and exocrine and endocrine secretion in the pig pancreas. 267 36


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