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)

Using radiolabeled microspheres, spinal cord blood flow was measured after spinal subarachnoid injections of 3.1- to 12.5-nmol doses of somatostatin through either indwelling i.t. catheters or acutely inserted intervertebral needles. With either injection technique, somatostatin caused significant dose-dependent reductions in thoracic and lumbosacral blood flow that could be partially blocked by a 5-min preinjection of the somatostatin receptor antagonist cyclo[7-aminoheptanoyl-Phe-D-Trp-Lys-Thr(Bzl)], which has previously been shown to block the hindlimb flaccidity produced by these doses of somatostatin in conscious rats. The duration of these blood flow changes were appreciably less in the rats injected through indwelling i.t. catheters. Somatostatin-induced reductions in spinal cord perfusion were accompanied by transient pressor responses, reduced cardiac output, 3-fold increases in spinal cord cerebrospinal fluid lactic acid concentrations and breakdown of the blood-spinal cord barrier, as reflected by significantly increased extravasation of [125I]bovine serum albumin. By 24 hr postinjection, a 12.5-nmol dose of somatostatin caused appreciable spinal cord cellular injury, as evidenced by significant elevations in cerebrospinal fluid concentrations of lactate dehydrogenase. After topical application to exposed pial vessels of the parietal cortex, comparable doses of somatostatin caused immediate intense dose-related arteriolar vasospasm and subsequent extravasation of the visible macromolecular tracer Evans blue dye. We conclude that somatostatin has significant vasoconstrictory effects on the blood vessels of the brain and spinal cord of the rat that must be recognized and appreciated when studying its neuropharmacological actions in vivo.
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PMID:Somatostatin causes vasoconstriction, reduces blood flow and increases vascular permeability in the rat central nervous system. 134 70

Somatostatin-14-like immunoreactivity (S14LI) and somatostatin-28(1-12)-like immunoreactivity (S28(1-12)LI) in the brain of LEC (Long Evans Cinnamon) rats with hepatic encephalopathy were measured. Significant reduction of both S14LI and S28(1-12)LI was observed in the hypothalamus, medulla oblongata, striatum and spinal cord. Both of the immunoreactivities in the hypothalamus of these rats were approx. 50% of those in LEC rats without hepatic encephalopathy. The amounts of reduction of S14LI significantly correlated with those of reduction of S28(1-12)LI. No significant difference in gel chromatographic profiles of S14LI and S28(1-12)LI was observed between LEC rats with and without hepatic encephalopathy. These results suggest that the reduction of somatostatin-like immunoreactivity in LEC rats with hepatic encephalopathy may be caused by a decrease in production of prosomatostatin rather than altered degradation.
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PMID:Reduced somatostatin-like immunoreactivity in the brain of LEC rats with hepatic encephalopathy. 168 62

Cardiovascular responses to intracerebroventricular (icv) injections of substance P and somatostatin were measured in Long-Evans and Brattleboro rats treated with streptozotocin (STZ) or saline. Substance P icv evoked similar pressor responses and tachycardia in STZ-treated and saline-treated Long-Evans rats, together with signs of behavioral activation (i.e., arousal). As a group, Brattleboro rats did not respond significantly to icv substance P, although some individual rats showed clear cardiovascular and behavioral responses. These findings may indicate a reduced sensitivity to icv substance P in Brattleboro rats but show no differences attributable to STZ treatment. Hence, diminished pressor responses to icv angiotensin II (observed previously) may be specific to sympathoadrenal activation associated with drinking. Somatostatin caused a pressor effect in saline-treated, but not in STZ-treated, Long-Evans rats, which was probably due to arginine vasopressin (AVP)-mediated mechanisms because it was not present in either saline-treated or STZ-treated Brattleboro rats. Both control and STZ-treated Long-Evans rats showed a bradycardic response to somatostatin that was not seen in Brattleboro rats. These results indicate that different AVP-mediated mechanisms might be responsible for the pressor and bradycardic effects of icv somatostatin. It is possible that impairment of central somatostatin-mediated AVP release contributes to the diminished role of AVP in blood pressure recovery following ganglion blockade in STZ-treated rats described previously.
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PMID:Central effects of substance P and somatostatin in conscious, streptozotocin-treated rats. 169 38

Somatostatin (SRIF) receptors are expressed in the external granule cell layer of the rat cerebellum during early postnatal life. The aim of the present study was to investigate the distribution and biochemical characteristics of SRIF binding sites in the cerebellum of homozygous (vasopressin deficient) Brattleboro rats, which exhibit a selective impairment of their granule cell layer. This study has been conducted in 13-day-old rats by means of membrane-binding assay and autoradiography using [125I-Tyr0,DTrp8]S14 as a radioligand. In the cerebellum of homozygous Brattleboro rats, Scatchard plot analysis revealed the existence of a single class of SRIF receptors with similar Kd values as in Long-Evans or heterozygous Brattleboro rats (180-200 pM). Conversely, a marked reduction of the concentration of SRIF binding sites was observed in Brattleboro rats as compared to heterozygous or Long-Evans rats. In homozygous Brattleboro rats, autoradiographic studies revealed that the concentration of SRIF receptors was reduced in all lobules of the cerebellum as compared to Long-Evans. In addition, the magnitude of the decrease of receptor concentration was greater than the loss of granule cells observed in the homozygous Brattleboro rat. These results indicate that the expression of SRIF receptors by immature granule cells of the cerebellum is markedly reduced in Brattleboro rats. Whether the impairment of SRIF receptors in diabetes insipidus rats can directly be ascribed to vasopressin deficiency remains to be determined.
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PMID:Expression of somatostatin receptors is impaired in the cerebellum of developing Brattleboro rats. 198 Aug 50

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.
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PMID:Changes in oxytocin and vasopressin content in posterior pituitary and hypothalamus following pantethine treatment. 240 77

The retinas of adult, male Long-Evans rats contain somatostatin-like immunoreactive material (SLI) as detected by radioimmunoassay. The SLI co-chromatographs with synthetic somatostatin-14 on both gel permeation chromatography and reversed phase high performance liquid chromatography; no somatostatin-28-like material or higher molecular weight forms have been detected. Immunocytochemical methods detect SLI in at least two cell populations. The more abundant stained cells are at the inner margin of the inner nuclear layer and give off processes which form a dense meshwork of fine, varicose fibers at the outer border of the inner plexiform layer, as well as processes which pass into other sublaminas of the inner plexiform layer. Varicose immunoreactive fibers run vertically or obliquely through the inner nuclear layer and bifurcate at its outer margin, giving rise to horizontally running fibers in the outer plexiform layer. These observations are consistent with rat retinal SLI being contained within amacrine cells, at least some of which are interplexiform cells. With cholchicine pretreatment, a more sparse population of stained cells is detected in the ganglion cell layer. These cells give rise to processes which enter the inner plexiform layer. It is not known if these are ganglion cells or displaced amacrine cells.
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PMID:Immunoreactive somatostatin in the rat retina: light microscopic immunocytochemistry and chromatographic characterization. 240 7

To investigate whether somatostatin systems plays a significant role in the regulation of the hypothalamic-pituitary-adrenal axis, the effects of cysteamine, a drug which reduces somatostatin levels, on the dexamethasone-induced suppression of plasma corticosterone levels were examined in the rat. Male Long Evans rats were handled daily for 1 week prior to receiving a standard dexamethasone suppression test. On the 1st day, rats received a 9.00 a.m. saline injection and blood samples were taken from the tail at 1.00 p.m. On the 2nd day, rats received dexamethasone or saline at 9.00 a.m. and a second blood sample was taken at 1.00 p.m. Experimental groups were pretreated with systemic injections of cysteamine, 5 min or 14 h, prior to receiving dexamethasone. Additional groups, previously implanted with guide cannulae, were given an infusion of cysteamine or saline into the lateral ventricle 14 h prior to dexamethasone. Circulating corticosterone levels were determined by radioimmunoassay. Rats were sacrificed immediately following each experiment and the hypothalamus dissected and assayed for levels of somatostatin immunoreactivity. The results of the first experiment showed that dexamethasone (10 micrograms/kg) alone reduced plasma corticosterone levels from control values (174 +/- 36 ng/ml) to undetectable levels (less than 25 ng/ml). Pretreatment with cysteamine 5 min prior to dexamethasone, while having no significant effect on basal corticosterone levels, completely blocked the dexamethasone-induced suppression of corticosterone levels. Similar observations were obtained with rats pretreated with cysteamine 14 h prior to dexamethasone. In contrast, intracerebroventricular cysteamine pretreatment did not block the dexamethasone-induced suppression of corticosterone levels. These results add further evidence in support of an involvement of somatostatin systems in the regulation of the hypothalamic-pituitary-adrenal axis.
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PMID:Effects of systemic and intracerebroventricular cysteamine on dexamethasone-induced suppression of corticosterone levels in the rat. 290 61

Spontaneously occurring neoplasms and non-neoplastic proliferative changes of the pancreatic cells in aging Sprague-Dawley and Long-Evans rats were examined for the presence and distribution of pancreatic hormones using immunocytochemical techniques. Islet cell tumors were indistinguishable in the two rat strains. They were composed principally of insulin-containing beta cells, but had additional and variable small proportions of cells that stained for somatostatin, glucagon, or rarely, pancreatic polypeptide. The heterogeneity in these spontaneous islet cell neoplasms was similar to that reported in humans as well as those induced in rats by streptozotocin. Hyperplasia of the islet cells also mainly affected the beta cells, but the overall pattern of immunocytochemical staining usually remained similar to that of normal islets, a point of distinction from islet cell neoplasms. In addition, rats with exocrine atrophy and fibrosis were found to have considerable disruption and focal proliferation of the islets.
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PMID:Neoplasia and hyperplasia of pancreatic endocrine tissue in the rat: an immunocytochemical study. 300 1

The distribution of vasoactive intestinal polypeptide (VIP), gastrin-releasing peptide (GRP)/bombesin, somatostatin, vasopressin, neuropeptide Y (NPY) and serotonin was examined immunohistochemically in the suprachiasmatic nucleus (SCN) of male rats genetically deficient for vasopressin (Brattleboro strain). VIP-containing neurons and their varicose fibers were preferentially distributed in large numbers in the ventromedial part of the SCN. GRP/bombesin-containing neurons and their fibers were also gathered in the ventral part of the SCN, particularly in the ventromedial region of the nucleus. Somatostatin-containing neurons and their fibers were prominent in the rostral and middle portions of the SCN, where the highest concentration of immunoreactivity was restricted in their ventromedial part. No vasopressin-immunoreactivity was found at all throughout the SCN. Profuse NPY-containing varicose fibers were observed in the ventrolateral part of the SCN, but no immunoreactive neurons were distributed in this nuclear region. Serotonergic fibers showed a topographic arrangement in the SCN: a serotonin-immunoreactive nerve plexus was predominantly distributed in the ventrolateral part. These findings indicate that the SCN of Brattleboro rats is composed of distinct subdivisions of immunoreactive cell bodies and fibers. The distribution of the five peptides and indoleamine within the SCN in the Brattleboro strain was compared with that in normal Long-Evans rats. Furthermore, both strains of rats were exogenously administered with arginine-vasopressin, but no conspicuous difference in the regional patterns of immunoreactivity was detected. The possible role of vasopressin in the SCN is discussed.
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PMID:Immunohistochemical studies on the distribution of neuropeptides and serotonin in the suprachiasmatic nucleus of the Brattleboro rat. 361 94

Somatostatin content was studied in brain nuclei and pituitary lobes of homozygous Brattleboro rats lacking vasopressin (DI rats) with and without vasopressin replacement, and their corresponding controls, heterozygous Brattleboro (HZ) rats and Long-Evans (LE) rats. High, vasopressin-reversible, somatostatin levels occurred in DI rats. The changes in somatostatin were localized to the nucleus periventricularis and to brain areas receiving somatostatin projections from this nucleus, including the eminentia mediana. In contrast, vasopressin administration failed to alter somatostatin levels in HZ rats. In brain areas not belonging to the somatostatin periventricular system, the peptide concentration in DI rats was not higher than that of LE controls. High somatostatin levels were present in the intermediate lobe of the pituitary gland. Somatostatin was higher in DI and HZ rats when compared to LE rats. In the posterior pituitary lobe, HZ rats had higher, and DI rats lower, somatostatin than control LE rats. These results suggest that rat brain and pituitary vasopressin and somatostatin systems are interrelated.
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PMID:High, vasopressin-reversible, immunoreactive somatostatin in specific hypothalamic nuclei of rats with diabetes insipidus (Brattleboro rats). 613 44


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