UNIPROT:P61278 - FACTA Search

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Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the membrane potential and the intracellular Ca2+ concentration ([Ca2+]i) caused by somatostatin (SRIF) were simultaneously measured in human GH-producing pituitary tumor cells, by means of the nystatin-perforated whole cell clamp technique and Fura-2 AM. An application of 10(-8) M SRIF hyperpolarized the membrane and arrested Ca(2+)-dependent spontaneous action potentials. [Ca2+]i concurrently decreased during membrane hyperpolarization. When the membrane potential was clamped below the threshold for voltage-gated Ca2+ channels, [Ca2+]i decreased and SRIF did not further reduce [Ca2+]i. In cells which did not show spontaneous action potentials, SRIF hyperpolarized the membrane but it affected [Ca2+]i little. From these results it was concluded that the reduction in [Ca2+]i caused by SRIF was ascribed to the decrease in Ca2+ influx through voltage-gated channels during membrane hyperpolarization. The effect of SRIF on the voltage-gated Ca2+ channel current was also examined under the perforated whole cell clamp. SRIF (10(-8) M) inhibited the Ca2+ channel current to 80.8 +/- 15.4% (n = 5) of the control. Because SRIF-induced inhibition of the voltage-gated Ca2+ channel current was not prominent, it was considered that membrane hyperpolarization is the major cause of the reduction in [Ca2+]i in human GH-producing cells.
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PMID:Simultaneous measurement of changes in the membrane potential and the intracellular Ca2+ concentration caused by somatostatin in human GH-producing pituitary tumor cells. 136 50

Calcitonin (CT) secretion is not exclusively controlled by calcemia, but the secretory tonus is maintained by the beta-stimulatory adrenergic system Somatostatin (SMS) plays a neuromodulatory role with the reduction of CT secretion by its interference at the central and peripheral level of the beta adrenergic receptors. The experiments were carried out on groups of rats in which the effect of SMS on CT content of the thyroid gland was followed up. Thus, SMS administered i.c.v. significantly reduced the basal CT secretion without blocking the stimulatory effect of calcium. The results were comparable with those obtained after the blockade of the sympatho-adrenergic system by chemical sympathectomy with 6HODA or propranolol. Central blockade of alpha receptors with phentolamine determined a significant rise of CT. This effect was annihilated by SMS. The i.v. administration of SMS did not induce a change in CT content of the thyroid, but blocked the stimulatory action of hypercalcemia. The results are identical with those obtained by blocking the beta-receptors with propranolol. SMS also blocked the stimulatory effects of isoproterenol on CT secretion. The data obtained revealed the fact that SMS lowers CT secretion by the central and peripheral interference of the sympatho-adrenergic path, maintaining the secretory tonus of the thyroid C cells.
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PMID:Inhibitory role of somatostatin on calcitonin secretion. 136 72

1. The objective of the present study was to evaluate the electrophysiological effects of the peptide somatostatin (SST) at the supraventricular level in isolated guinea pig hearts. 2. ECG recording from isolated hearts perfused by the Langendorff method indicated that 1.0 microM SST induced a decrease in heart rate from 174 +/- 15 to 157 +/- 9 bpm (N = 6, P < 0.05), blocked AV conduction (the PR interval increased from 92 +/- 11 ms to 106 +/- 5 ms, N = 5, P < 0.05) and increased the QTc interval from 210 +/- 0 to 232 +/- 4 ms (N = 5, P < 0.05). The supraventricular effects of SST, particularly upon the AV conduction, were potentiated by a reduction in calcium concentration from 2.5 to 0.5 mM in the perfusing solution. Thus, 1.0 microM SST induced 2nd degree AV conduction block progressing to AV dissociation in 75% of the hearts in the low calcium medium instead of the first degree conduction block observed in all hearts in normal calcium medium. 3. His bundle electrogram evidenced a complete A-H dissociation without significant change in the H-V interval and microelectrode studies showed a complete abolition of the AV node action potential in the presence of 1.0 microM SST. Both results demonstrate that the site of AV conduction block induced by SST is at the AV node. 4. All the supraventricular effects of SST were transitory, subsiding within about 10 min of hormone exposition, showing desensitization. 5. The effects of somatostatin here described were not blocked by 10 microM atropine, indicating that they are not mediated by muscarinic receptors. 6. These data provide a direct electrophysiological demonstration of the supraventricular effects of SST, and suggest that this peptide decreases calcium influx during the action potential.
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PMID:Electrophysiological effects of somatostatin at the supraventricular level of isolated guinea pig hearts. 136 35

The effects of somatostatin and alpha 1-adrenergic receptor agonists on cytosolic Ca2+ in striatal astrocytes from the embryonic mouse in primary culture have been investigated by microfluorimetry. Methoxamine or somatostatin induced a transitory increase in cytosolic Ca2+, but their combined addition led to a sustained increase in cytosolic Ca2+ which seems to be due to a Ca2+ influx since it was not observed in the absence of external Ca2+. Voltage-independent Ca2+ channels contribute to this process. Indeed, voltage-operated calcium channels are not involved since neither dihydropyridines nor La3+ were effective in suppressing the sustained cytosolic Ca2+ elevation. Moreover, depolarization by 50 mM KCl, which was ineffective alone, suppressed the effect of somatostatin observed in the presence of the alpha 1 agonist, methoxamine. The implication of arachidonic acid in the observed potentiation is suggested by the following observations: 1) arachidonic acid induced a sustained elevation of cytosolic Ca2+ similar to that evoked by the co-application of methoxamine and somatostatin; 2) the addition of ETYA, an inactive and non-metabolizable analogue of arachidonic acid suppressed the calcium plateau produced by the agonists. In addition, direct activation of PKC by an exogeneous diacylglycerol analogue allowed somatostatin alone to evoke a sustained elevation of cytosolic Ca2+. Therefore, methoxamine through the successive activation of PLC and PKC could allow a lipase, probably PLA2, to be stimulated by somatostatin. Since arachidonic acid has already been shown to trigger the opening of K+ channels and the formation of inositol phosphates, somatostatin, through the arachidonic acid-mediated hyperpolarization could increase the Ca2+ driving force and thus improve Ca2+ influx through the inositol phosphate gated channels.
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PMID:Synergistic regulation of cytosolic Ca2+ concentration by somatostatin and alpha 1-adrenergic agonists in mouse astrocytes. 136 95

Somatostatin and muscarinic acetylcholine receptors are similar as far as modulation of voltage-gated Ca2+ channels and anomalously rectifying K+ channels are concerned. Activation of either type of receptors induces inhibition of Ca2+ channels and activation of anomalous K+ channels without depending on intracellular cAMP. Somatostatin appears to act on the same receptor subtype for these two actions since somatostatin receptors are homogenous in pituitary cells (Srikant and Patel, 1982; Tran et al., 1985) where the peptide produces these two effects as well as an inhibition of adenylate cyclase. In the case of muscarinic receptors, however, it remains unclear whether the same subtype of receptors is involved in both inhibition of Ca2+ channels and activation of K+ channels. Activation of muscarinic receptors in hippocampal neurones evidently produces a cAMP-independent suppression of Ca2+ channel. In cardiac cells, however, muscarinic stimulation does not cause a cAMP-independent suppression of Ca2+ channels but does activate an anomalous rectifier. These findings do not necessarily mean that the muscarinic receptor involved in the inhibition of Ca2+ channels in hippocampal neurones is not of m2 type which is assumed to mediate the activation of anomalous K+ channels in cardiac cells. There is no evidence that cardiac Ca2+ channels are identical to hippocampal Ca2+ channels susceptible to muscarinic inhibition. In addition, a similar argument could be applied to G proteins coupling muscarinic receptors to Ca2+ channels in neurones and cardiac myocytes. In this regard, it should be noted that activation of GABAB receptors or mu and delta opiate receptors, an event known to inhibit adenylate cyclase activity through a PTX-sensitive Gi protein, also produces both inhibition of Ca2+ channels and activation of anomalous K channels in a cAMP-independent manner. This close correlation between inhibition of adenylate cyclase activity and cAMP-independent modulation of Ca2+ and K+ channels suggests the possible involvement of m2 subtype in the inhibition of Ca2+ channels in hippocampal neurones. Circumstantial evidence indicates that anomalous K+ channels are directly activated by alpha subunits of Gi, but not Go, proteins. The alpha subunit of Go protein seems to mediate inhibition of the Ca2+ channel, probably in a direct manner. The most striking difference between somatostatin and muscarinic receptors would be their opposite actions on the M channel. All the inhibitory receptors on the M channel, including m1 and m3 receptors, are known to stimulate PI hydrolysis via a PTX-insensitive G protein.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Modulation of ion channels by somatostatin and acetylcholine. 137 25

The prophylactic effect of perioperative use of somatostatin on postoperative increase of pancreatic digestive enzymes was investigated in this double blind, randomized study. Thirty three patients undergoing pancreatic surgery because of chronic pancreatitis were divided randomly into two groups. Fifteen patients received somatostatin- (dose 125 micrograms/hour), 18 placebo-infusion, pre- and postoperatively for a total time of 48 hours. The level of serum amylase, lipase, gammaGT, calcium, creatinine and blood glucose was determined every 12 hours. In the placebo group the serum lipase and amylase increased significantly (p less than 0.001), while the calcium decreased. In the somatostatin treated patients only the lipase level increased significantly (p less than 0.01), while the amylase and calcium showed no significant changes compared to their initial values. The postoperative increase in serum enzyme levels is interpreted as being an indicator of pancreatic injury. These results suggest that the perioperative use of somatostatin has beneficial effect for the prevention of pancreatic enzymes increases, associated with pancreatic surgery or its complications in patients with chronic pancreatitis.
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PMID:[Somatostatin in the prevention of postoperative increase of pancreatic enzyme after pancreatic surgery]. 137 31

The effect and mode of action of vasoactive intestinal polypeptide (VIP), a peptidergic neuromodulator in the gastrointestinal nervous system, were investigated in isolated muscle strips of the guinea-pig ileum. VIP induced concentration-dependent (20 nM-1 microM) contractions of longitudinal ileal strips. TTX (1 microM), a mixture of atropine (3 microM) and spantide (30 microM), a mixture of atropine (3 microM) and omega-conotoxin GVIA (100 nM), somatostatin (60 nM) and dynorphin (100 nM) abolished the effect of VIP. In most cases a small relaxation became evident. Desensitization to substance P in the presence of atropine prevented VIP-induced contraction. A partial inhibition was observed in the presence of atropine (3 microM), spantide (30 microM), omega-conotoxin GVIA (100 nM), beta-endorphin (265 nM), met-enkephalin (1100 nM) and a mixture of spantide (30 microM) and omega-conotoxin GVIA (100 nM). The action of VIP was not significantly modified by guanethidine (3 microM) or hexamethonium (150 microM). In circular ileal strips VIP (10-300 nM) caused concentration-dependent relaxations through a direct myogenic effect. These results indicate that the VIP produced contractions of the guinea-pig ileum are exclusively neurally mediated and involve a cholinergic as well as a noncholinergic-nonadrenergic (NANC) pathway. It is concluded that besides acetylcholine (Ach) VIP releases the peptidergic transmitter substance P from postganglionic nerve fibers of myenteric plexus. Opioid peptides and somatostatin modulate the activity of cholinergic and peptidegic nerves in the guinea-pig ileum. The release of substance P appears to depend completely on N-type voltage sensitive calcium channels.
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PMID:Vasoactive intestinal polypeptide induces neurogenic contraction of guinea-pig ileum. Involvement of acetylcholine and substance P. 137 93

Retinal bipolar cells are non-spiking interneurons that relay information from photoreceptors to amacrine and ganglion cells. In turn, bipolar cells receive extensive synaptic feedback from amacrine cells, some of which contain neuropeptides, including substance P. We have examined the effect of substance P on single bipolar neurons isolated from goldfish retina and find that substance P (0.1-1 nM) produced a voltage-dependent inhibition of calcium current in these cells. The inhibition was strongest at negative potentials, with the peak suppression occurring at -20 to -30 mV; at potentials positive to 0 mV, there was little effect on calcium current. Thus, the net effect was to shift the voltage range of activation of calcium current toward more positive potentials. The inhibition of calcium current by substance P required GTP in the patch pipette and was blocked by internal GDP-beta-S. Similar effects on calcium current were observed with somatostatin and metenkephalin, which are also found in amacrine cells.
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PMID:Substance P modulates calcium current in retinal bipolar neurons. 137 97

The regulation of steady state levels of follistatin (FS) messenger RNA (mRNA) was examined in a rat renal mesangial cell line in tissue culture. A specific 32P-radiolabeled antisense probe was used which corresponds to the 3' end of exon 5 together with the 5' end of exon 6 of the rat FS gene, and which distinguishes between the two different forms of FS mRNA. In addition, a specific 35S-radiolabeled probe for the ubiquitous protein cyclophilin was developed and used as an internal standard. Total RNA was harvested from confluent cell cultures to yield four independent samples per treatment/time point, and equal amounts of RNA from every sample in a given experiment were subjected to S1-nuclease analysis for the estimation of specific mRNA levels. Treatment of the cultured cells with epidermal growth factor (10 nM) caused an 8- to 9-fold increase in the FS mRNA level after 4 h, but no consistent change was observed after treatment with basic fibroblast growth factor (0.28 or 0.56 nM), somatostatin (3.7-73 nM), angiotensin II (0.1-2500 nM), or FS itself (0.29 nM) for between 4 and 48 h. Neither activin (0.5 or 1.2 nM) nor inhibin (0.64 nM) changed the FS mRNA level in the mesangial cell line during a 24-h treatment. FS mRNA levels in the cells also were not affected by a 48-h treatment with the steroids dihydrotestosterone (1-1000 nM), estradiol (1 and 100 nM), and the antiprogesterone RU 486 (1000 nM), whereas 100 nM RU 28362 (a synthetic glucocorticoid) caused a 5- to 6-fold increase and 1000 nM progesterone increased the FS mRNA level up to 3.5-fold above control. Retinoic acid, a vitamin A derivative, significantly increased the FS steady state mRNA level at 3 nM, and at 1000 nM stimulated FS mRNA up to 5-fold within 4 h, whereas incubation of the cells with 30 microM prostaglandin E2 for 4 h caused a 10-fold increase. The FS mRNA level increased 3- and 4-fold within 4 h during incubation of the cells with 100 nM phorbol 12-myristate, 13-acetate, and 25 microM forskolin, respectively, whereas the calcium ionophore A23187 (1-100 microM) caused no change within this timespan. None of the tested hormones had an obvious effect on the ratio of the two different forms of FS mRNA (FS 344:FS 317).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Follistatin steady state messenger ribonucleic acid levels in confluent cultures of a rat renal mesangial cell line are regulated by multiple factors. 137 7

We evaluated the effect of seven classes of neuropeptides [bradykinin, cholecystokinin 26-33 (CCK), neurotensin, arginine-8 vasopressin (AVP), tyr-4 bombesin (BN), somatostatin, and motilin] on 18 human lung cancer and four human breast cancer cell lines to determine the pattern of responses. Flow cytometric analysis of Indo-1 AM-loaded cells was used to quantitate the intracellular calcium response of individual cells produced by these peptides alone or in simultaneous or sequential combinations. All 18 lung cancer cell lines responded to one or more peptide classes with classic small cell lines displaying the greatest responsiveness, followed by variant small-cell lines and non-small-cell lung cancer cell lines. Breast cancer cell lines demonstrated little or no response to any peptide. There was great variability in the magnitude of response and pattern of response in individual cell lines and between cell lines. Bradykinin was the most potent peptide and produced responses in the largest number of lung cancer cell lines. Simultaneous administration of active peptides produced greater intracellular calcium release than single peptides, though in a less than additive manner. Response to each peptide was followed by a refractory period lasting several hours or more. The refractoriness was peptide-specific, implying that each peptide has a distinct pathway, at least at the receptor level. Bradykinin antagonists could abrogate the calcium response to bradykinin but not to other peptides. Similarly, specific peptide antagonists for CCK, BN, and AVP blocked the response for only their specific agonist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of neuropeptides on human lung and breast cancer cells. 138 87

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