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

Substance P stimulation of salivation in rats has been studied as has its in vitro enhancement of amylase release by isolated parotid cells. The extent of the stimulation on amylase release by isolated parotid cells was dependent upon the concentration of substance P, with the minimum effective concentration being 1 nM. The substance P effect was detectable within 1 min after incubation and lasted for at least 50 min. Substance P stimulation was demonstrable at 25--37 degrees C but not at 0 degrees C. Adrenocorticotropic hormone (ACTH), thyrotropin-releasing hormone (TRH), vasopressin and neurotensin had no effect on amylase release. These results suggest that substance P may act directly on the parotid cells. Examination of the salivary-stimulating activity of fragments of substance P showed that the C-terminal octapeptide and (pyroglutamyl)hexapeptide were active, although less potent than substance P, whereas its free acid, C-terminal tetra- and tri-peptides were inactive. Vasopressin, angiotensin II and neurotensin could inhibit substance P induced salivation, whereas TRH, ACTH and somatostatin had no effect. Amylase activity per unit volume of saliva was not changed by the injection of vasopressin, angiotensin II or neurotensin. These vasoactive peptides did not affect substance P stimulation of amylase release by isolated parotid cells. The results indicate that vasopressin, angiotensin II and neurotensin inhibit the action of substance P on salivation at sites other than the parotid cells.
 ...
PMID:Substance P stimulation of amylase release by isolated parotid cells and inhibition of substance P induction of salivation by vasoactive peptides. 22 41

Intraventricular injection of arginine-8-vasopressin and its analogues vasotocin and lysine-8-vasopressin into rat brain evoked a special rotational behavior resembling somatostatin-induced barrel rotation [1]. Oxytocin and oxypressin were less active while vasopressin fragments had no effect. Vasopressin-induced barrel rotation was accompanied by pathological symptoms indicating a disturbance of muscle tone regulation and is considered to be a non-specific and toxic effect. This rotational behavior was not prevented by atropine, propranolol, phentolamine, methylsergide or haloperidol but was reduced by chlorpromazine, probably due to the latter's muscle relaxing activity.
 ...
PMID:Barrel rotation induced by vasopressin and related peptides in rats. 56 83

Vasopressin (VP) stimulates insulin secretion and inositol phosphate (InsP) production in clonal hamster beta cells (HIT) via a cyclic AMP-independent V1-receptor-mediated signal-transduction pathway. Somatostatin (SRIF) inhibited VP-stimulated insulin secretion, and the effects of SRIF were abolished by pretreatment with pertussis toxin. The Ca(2+)-channel blockers verapamil and nifedipine also inhibited VP-stimulated insulin secretion during 20 min incubations, but verapamil was ineffective at 2 min, and the effects of SRIF and nifedipine together were not addictive. SRIF failed to inhibit further the attenuated insulin response to VP in Ca(2+)-free medium. VP-stimulated InsP production was also inhibited by SRIF in a pertussis-toxin-sensitive manner. Whereas VP-stimulated insulin secretion was almost completely inhibited by SRIF at an equimolar concentration, VP-stimulated InsP production was much less sensitive to inhibition by SRIF, even at a 100-fold excess concentration. VP increased cytosolic Ca2+ in HIT cells loaded with fura 2, the fluorescent Ca2+ indicator. The increase was biphasic, with an initial rapid spike increase followed by a prolonged second phase. Both SRIF, at a concentration which inhibited VP-stimulated insulin secretion but not InsP production, and verapamil failed to inhibit the rapid spike increase in intracellular Ca2+, but did inhibit the second phase. We conclude that VP induces biphasic changes in cytosolic Ca2+, secondary to mobilization of intracellular Ca2+ and influx of extracellular Ca2+. SRIF inhibits insulin secretion by interrupting influx of extracellular Ca2+, likely by inhibiting Gi-subunit activity. Inhibition of VP-stimulated phosphoinositide hydrolysis, which is also pertussis-toxin-sensitive, may represent an additional mechanism of action of SRIF.
 ...
PMID:Somatostatin inhibits vasopressin-stimulated phosphoinositide hydrolysis and influx of extracellular calcium in clonal hamster beta (HIT) cells. 136 25

Although the mechanism initiating and maintaining variceal hemorrhage is not completely understood, there has been general agreement in recent years on the concept that variceal rupture occurs when the tension on the wall of the varices reaches a critical value (the rupture point) that leads to the leakage of the elastic components of the wall. If this hypothesis is true, the aim of pharmacological treatment should be to reduce variceal wall tension or to prevent any abrupt increase in this parameter. Some vasoconstrictor drugs are currently used in order to achieve these goals and in the attempt to stop the acute bleeding episode. All these agents decrease either portal pressure and azygos blood flow. Vasopressin although effective, has significant cardiac and gastrointestinal adverse effects that discourage its use. Combination with nitroglycerin reduces its adverse effects while maintaining or even enhancing the reduction in portal pressure. Glypressin, which acts as a slow-release preparation of vasopressin, has a longer duration of action and can be administered as single intravenous injections instead of continuous infusion. However, the similarity of effects of these drugs on systemic circulation leads to an overlapping spectrum of untoward effects. Somatostatin and the synthetic octapeptide octreotide display similar pharmacological effects on splanchnic hemodynamics but have a better tolerability profile. Thanks to its longer duration of action and ease of administration, octreotide could become the drug of choice for the early, pre-hospital management of bleeding varices. A different approach to the pharmacological treatment of variceal bleeding may be the use of compounds, like metoclopramide and domperidone, that increase the lower esophageal sphincter pressure (LESP), thereby reducing the inflow of blood flow into the submucous venous plexus of the esophagus and hence into the esophageal varices. However, more studies are needed before these compounds be considered a real alternative to the above established drugs.
 ...
PMID:Clinical pharmacology of active variceal bleeding. 136 76

To study the hemostatic effect of Sandostatin, a long-acting analogue of somatostatin, in acute variceal bleeding, a prospective randomized controlled trial comparing it with Vasopressin was conducted in 41 cirrhotic patients with esophageal variceal bleeding. Initial hemostasis was achieved within 6 hours in 75% of patients treated with Sandostatin and in 61.9% treated with Vasopressin. Recurrent bleed developed in 20% of patients in Sandostatin group and 46.2% in Vasopressin group following initial hemostasis. Complete control of bleeding for 24 hours was attained in 60% of the Sandostatin group and in 33.3% of the Vasopressin group. There was no statistically significant difference in both the rate of initial hemostasis and complete bleeding control. Hospital mortality was also similar in both groups. However, transfusion requirements were less (P less than 0.05) and side effects tended to be milder in patients treated with Sandostatin. In conclusion, Sandostatin is at least as effective as Vasopressin in the treatment of acute variceal bleeding, and carries less severe complications than Vasopressin does.
 ...
PMID:A prospective randomized controlled trial of sandostatin and vasopressin in the management of acute bleeding esophageal varices. 151 74

Variceal bleeding has a high mortality, as the majority of patients have cirrhosis, with hepatic coma, renal failure, ascites and clotting deficiencies as complicating factors. Bleeding varices must therefore be treated as an emergency. Resuscitation, endoscopic diagnosis and haemostasis are the cornerstones of treatment. Once bleeding varices have been identified, attempts to stop the bleeding must be made at once as this will lessen the chances of hepatic failure developing. Endoscopic sclerotherapy at the time of diagnosis is the best available treatment at present, although profusely bleeding varices can be difficult to see and inject. In these circumstances the passage of a Sengstaken tube should stop the bleeding, allowing later sclerotherapy to be successful. If rebleeding recurs and cannot be controlled, oesophageal transection with a stapling gun may be life-saving, although the varices may later recur and long-term endoscopic follow-up will be necessary. Portacaval shunting and the distal splenorenal shunt involve arduous surgery and are followed by a significant incidence of hepatic encephalopathy; they should be reserved for those few cases when simpler measures have failed, although shunts do lead to permanent decompression of the portal system. The acute variceal bleed may also be dealt with pharmacologically. Vasopressin, used in combination with nitroglycerin to lessen the harmful side-effects, is cheaper and as effective as terlipressin or somatostatin and its synthetic analogue octreotide. Several courses of injection sclerotherapy will be required to eliminate oesophageal varices. Thereafter, long-term follow-up will be necessary to deal with any recurrence. The place of non-selective beta-blockers is still contentious, but they do reduce portal pressure and may lessen the chance of rebleeding. There is also a growing role for hepatic transplantation, which not only eliminates the varices but also restores liver function to normal and greatly reduces the risk of subsequent hepatoma development.
 ...
PMID:The management of variceal bleeding. 168 66

Numerous cells containing P-450(F-1) were detected in the magnocellular and parvocellular neurons of the paraventricular nucleus of the hypothalamus. Electron microscopic analysis of immunoreactive neurons has shown that P-450(F-1) immunoreactivity is present on the Golgi apparatus and rough endoplasmic reticulum. In the paraventricular nucleus, the P-450(F-1)-positive magnocellular neurons frequently contained oxytocin and some of them also contained CRF. Vasopressin was colocalized with P-450(F-1), but these neurons did not express CRF. In the supraoptic nucleus, P-450(F-1) was colocalized with oxytocin or CRF in single neurons, but not with vasopressin. No cells exhibiting the colocalization of both P-450(F-1) and somatostatin were observed in these nuclei. The results of the present study concerning colocalization of P-450 and peptides suggest that P-450(F-1) is involved in the hypothalamo-hypophyseal neuroendocrine function in the female rat.
 ...
PMID:A sex-specific cytochrome P-450(F-1) colocalized with various neuropeptides in the paraventricular and supraoptic nuclei of female rats. 176 49

1. The use of radioactive and biotinylated oligonucleotide probes has been optimized to detect and analyze by in situ hybridization, neurons expressing neuropeptide genes (vasopressin, oxytocin, somatostatin). 2. In situ hybridization was performed on cryostat-cut sections obtained from tissues perfused with 1% formaldehyde. Radioactive probes were labeled by tailing with 35S-dATP and revealed with autoradiography. Biotinylated probes were obtained either by the incorporation of 11-biotin dUTP or by the addition of biotinylated nucleotides to the oligonucleotide during its synthesis. Biotin was revealed with streptavidin alkaline phosphatase and the appropriate substrate. 3. In the adult rat brain, radioactive and biotinylated probes revealed peptidergic neurons. The biotinylated probes provided an optimal cellular and subcellular resolution with a sensitivity similar to that observed with radioactive probes. Staining was selectively restricted to the cytoplasm and to the proximal part of processes. 4. Biotinylated vasopressin probes with 10 biotins added demonstrated magnocellular neurons and parvocellular neurons in the suprachiasmatic nucleus and the bed nucleus stria terminalis. 5. Vasopressin gene expression was studied during ontogeny in the rat fetus and neonate. Vasopressin mRNA was first detectable at gestational day 16 in the supraoptic nucleus in neurons of neuroblastic appearance. An aspect similar to the one present in adult was found at gestational day 19 in magnocellular neurons and at day 3 postnatal in parvocellular neurons. 6. The results confirm that radioactive oligonucleotide probes are efficient tools to investigate neuropeptide gene expression by in situ hybridization and demonstrate that biotinylated oligonucleotides are very efficient and provide a much higher resolution than radioactive probes with a reasonable sensitivity.
 ...
PMID:Topography and ontogeny of the neurons expressing vasopressin, oxytocin, and somatostatin genes in the rat brain: an analysis using radioactive and biotinylated oligonucleotides. 197 Jul 59

Pantethine, a cysteamine precursor, depletes somatostatin in the cerebral cortex and hypothalamus and prolactin in the anterior pituitary and hypothalamus. This study investigated the effect of pantethine on oxytocin and arginine vasopressin content in the posterior pituitary and hypothalamus. Male Long-Evans rats were injected intraperitoneally with escalating doses of pantethine (i.e., 146.7 mg, 293.4 mg and 586.6 mg/100 gm body weight). Hormone content was determined by radioimmunoassay. Three hours after pantethine treatment, the oxytocin content in the posterior pituitary and the hypothalamus was markedly reduced with all doses of the drug. Vasopressin content in the posterior pituitary and hypothalamus was decreased but to a lesser extent than oxytocin and only with the highest dose of pantethine. Pantethine may act to reduce oxytocin and vasopressin content through intracellular conversion to cysteamine. The exact mechanism of action of pantethine on oxytocin and vasopressin remains to be elucidated.
 ...
PMID:Changes in oxytocin and vasopressin content in posterior pituitary and hypothalamus following pantethine treatment. 240 77

Somatostatin and substance P (10(-6)-3 X 10(-5) M) inhibited dose-dependently the specific binding of [3H] [D-Ala2, Met5]enkephalinamide [( 3H]-DALAMID) to rat brain membranes, by decreasing the number of binding sites. [Lys]-Vasopressin also inhibited the binding, by affecting both the number of binding sites and the affinity of receptors to [3H]DALAMID. The results indicate that somatostatin and substance P may interfere with the endorphin system by an apparently competitive manner.
 ...
PMID:Somatostatin, substance P and [Lys]-vasopressin interfere with the binding of [3H][D-Ala2, Met5]enkephalinamide to rat brain membranes. 241 36


1 2 3 4 5 Next >>