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)

This article deals with the neuropeptides found in the eye and their actions. Substance P (SP) and VIP have been found in the anterior chamber of the eye. Here SP is localized in the sensory nerves of the sclera, cornea, iris, ciliary body and ciliary processes. It is supposed to be a sensory transmitter but can also be liberated by peripheral nerve endings as a response to various trauma. When this happens in the eye, for instance, after irritation of the Vth cranial nerve, SP causes an intense and long lasting miosis and may have some further actions as well. VIP has been demonstrated in nerves (probably cholinergic) of the posterior choroid and ciliary body. It is a potent vasodilator and may regulate choroideal blood flow. The retina is especially rich in different neuropeptides. SP, VIP, neurotensin, enkephalin, somatostatin, glucagon and gonadotropin-releasing hormone have all been demonstrated in the inner plexiform layer of the retina of various animal species. Specific information about the physiological role of retinal neuropeptides is still scarce but research is in progress. Considering the clinical significance of the new information about ocular neuropeptides, SP seems to be the most important substance. Recently a synthetic SP antagonist was reported to block the inflammatory response in the rabbit eye, which suggests a clinical use for this type of compounds.
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PMID:Ocular neuropeptides. 617 9

The effects of capsaicin, the major pungent ingredient of hot peppers, were assessed on sensory neuron neuropeptide levels and on sensory function in the adult guinea pig. Systemic doses of capsaicin as low as 2.5 mg/kg depleted substance P (SP) in dorsal roots plus ganglia (DRG) whereas a 10-mg/kg dose depleted the peptide maximally in DRG and in the dorsal spinal cord. High doses of capsaicin had no consistent effects on levels of cholecystokinin (CCK), vasoactive intestinal polypeptide, or somatostatin, although a transient decrease in CCK levels was observed 4 days after dosing. A single 5-mg/kg dose of capsaicin rendered animals completely insensitive to chemical irritation of the cornea without affecting sensitivity to noxious heat. Higher doses of capsaicin produced a marked insensitivity to nociceptive and non-nociceptive heat as well as to chemical irritation without affecting other sensory modalities. The SP depletion and sensory deficits produced by a single 50-mg/kg dose of capsaicin were still evident 10 weeks later. The pattern of selectivity of the sensory deficits produced by capsaicin differed from that produced by morphine which was active against all forms of nociceptive stimuli. The results indicate that in the guinea pig capsaicin is potent at producing a unique, long-lasting syndrome of peripheral sensory deficits that may result from an effect of the agent on SP-containing primary afferent neurons.
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PMID:Characterization of the peptide and sensory neurotoxic effects of capsaicin in the guinea pig. 619 77

Immunohistochemical studies on rats showed cysteamine to deplete immunoreactive somatostatin, but not substance P, in the substantia gelatinosa of the spinal trigeminal nucleus and spinal cord. The effect of cysteamine treatment on chemical pain was investigated using capsaicin as the pain-producing stimulus. Thermal pain was assessed with a hot plate test after cysteamine treatment. It was found that cysteamine did not alter the hind paw lick latency in the hot plate test or the number of forepaw wipes after application of a drop of capsaicin into the cornea, compared to normal animals. In capsaicin-treated animals a significantly lower number of forepaw wipes were seen after corneal capsaicin application. However, in cysteamine-treated animals slower wiping was observed compared to untreated and capsaicin-treated animals. This suggests that somatostatin may be of importance for the modulation of nociceptive information, although it is not a major pain transmitter.
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PMID:Effects of cysteamine on pain behaviour and on somatostatin- and substance P-like immunoreactivity in the substantia gelatinosa of the rat. 620 49

The influence of somatostatin and the potent mu-opiate receptor agonist etorphine on adrenal and autonomic responses mediated by trigeminal neurons was examined in chloralose-anesthetized cats. Microinjections of somatostatin (100 pmol) into laminae I-II of trigeminal subnucleus caudalis (Vc) evoked increases in the adrenal secretion of catecholamines and adrenal blood flow without affecting arterial pressure, heart rate, or plasma adrenocorticotropic hormone. Injections of somatostatin into laminae III-IV of Vc had no effect. Microinjections of etorphine (500 pmol) into laminae I-II of Vc had no effect, whereas injections into laminae III-IV caused small increases in total adrenal blood flow and peripheral concentrations of norepinephrine. To assess local effects of these drugs on peripheral trigeminal nociceptor-evoked autonomic responses, corneal stimulation was presented before and after topical application of somatostatin or etorphine on the dorsal brain stem surface. Somatostatin did not affect the adrenal and autonomic responses evoked by noxious thermal or chemical irritant stimulation of the cornea. Topical etorphine blocked completely the increase in adrenal blood flow, arterial pressure, and heart rate after noxious thermal stimulation of the cornea. These results suggest that somatostatin and mu-opiate receptor agonists act by different mechanisms at the level of the spinal trigeminal complex to affect adrenal and autonomic function.
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PMID:Central trigeminal effects of somatostatin and etorphine on adrenal and autonomic function in the cat. 878 Feb 31

Uncontrolled study has demonstrated the usefulness of somatostatin in the treatment of mild Graves' ophthalmopathy (GO). We performed a prospective study to evaluate the usefulness of somatostatin as compared to corticosteroid in the treatment of moderately severe GO. All patients were rendered euthyroid and observed for 3 months to exclude spontaneous improvement without active treatment. They were randomized to receive either somatostatin (SS, octreotide 200 micrograms q8h subcutaneously, n = 8) or corticosteroid (CS, prednisone 1 mg/kg/day in decreasing doses, n = 10). Assessments of soft tissue inflammation, exophthalmos, palpebral aperture, intraocular pressure, diplopia, cornea, and visual acuity were made every 4 weeks for 3 months. MRI of the orbit was performed before and after treatment. Both SS and CS therapy decreased the palpebral aperture and activity score after 3 months (p < 0.05), but those treated with CS had a lower activity score after treatment when compared to SS [2.5 (1-7) v.s. 3.5 (0-4), median (range), p < 0.05]. Only CS, but not SS, was able to reduce intraocular pressure and muscle size as documented by MRI, but no significant reduction in proptosis was observed in either group. Also, patients' self-assessments of the eye changes after treatment were similar between the two groups. Both groups showed significant elevation of urinary glycosaminoglycan (GAG) excretion before therapy (SS 24.6 +/- 10.8; CS 27.8 +/- 11.4 mg/24 h), which was reduced after treatment (SS 12.5 +/- 7.3; CS 10.8 +/- 6.3 mg/24 h, p < 0.05). However, no significant correlation could be observed between the degree of GAG reduction and the clinical outcome of the patients. In conclusion, the long acting SS octreotide was effective in reducing soft tissue inflammation and providing symptomatic relief in GO but not as effective as corticosteroid in reducing muscle size. In view of the minimal side-effects and similar efficacy as compared to corticosteroid in patients with minimal extraocular muscle enlargement, it is suggested that a trial of SS may be considered in selected patients with GO.
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PMID:The effect of somatostatin versus corticosteroid in the treatment of Graves' ophthalmopathy. 922 22

Corneal nerves regulate corneal epithelial integrity, proliferation, and wound healing. The mechanisms by which the nerves mediate their effects remain poorly understood; however, the release of biologically active neuropeptides has been hypothesized. The purpose of the current investigation was to determine the relative densities, distribution patterns, and origins of rat corneal nerves containing each of eight different neuropeptides, calcitonin gene-related peptide (CGRP), substance P (SP), galanin (GAL), neuropeptide Y (NPY), methionine-enkephalin (M-ENK), vasoactive intestinal polypeptide (VIP), somatostatin (SOM), and cholecystokinin (CCK). In the first set of experiments, immunohistochemical demonstrations of the above neuropeptides were performed on free-floating corneal sections cut tangential to the corneal surface. The results showed that six of the peptides, CGRP, SP, GAL, NPY, M-ENK, and VIP were present in rat corneal nerves. The innervation patterns of corneal nerves containing each of these six peptides were then documented by mapping all fibers in serial sections from select corneal quadrants onto a series of line drawings by using a drawing tube. In the second set of experiments, the origins of the corneal peptidergic nerve fibers were determined by selective ocular denervations. Unilateral combined sensory and sympathetic ocular denervations or unilateral sympathetic ocular denervations were performed in adult rats by transecting the ophthalmomaxillary nerve and/or removing the superior cervical ganglion. After 5-7 days, each of the ipsilateral corneas was sectioned and processed immunohistochemically for the presence of one of the six peptides found in experiment one, and the fibers that survived the ocular denervations were plotted onto line drawings. Ocular denervations revealed that corneal peptidergic nerves have sensory (CGRP, SP, and GAL), sympathetic (NPY), and parasympathetic (GAL, NPY, M-ENK, and VIP) origins. The results of this investigation have shown that the peptidergic innervation of the rat cornea is more extensive and complex than previously reported. This is the first investigation to show the presence of GAL in the rat cornea, and the first to demonstrate the presence of NPY-, VIP-, and M-ENK-IR nerve fibers in the cornea of any species.
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PMID:Peptidergic innervation of the rat cornea. 959 36

The present study investigates the effect of the somatostatin analogue octreotide acetate (SMS 201-995) on experimental angiogenesis in vitro and in vivo. Octreotide reduced the proliferation of human HUV-EC-C endothelial cells (mean, -45.8% versus controls at 10(-9) M; P < 0.05) as well as the density of the vascular network of the chick chorioallantoic membrane (mean, -35.7% versus controls at 50 microgram; P < 0.05). Furthermore, octreotide significantly inhibited chick chorioallantoic membrane neovascularization by the human MCF-10Aint-2 mammary cells secreting the angiogenic protein FGF-3. The proliferation of endothelial and smooth muscle cells from rat aorta explants on fibronectin was reduced by octreotide 10(-8) M (mean, -32.6% versus controls; P < 0.05), and a similar effect was produced on cells sprouting from explants cultured in fibrin (mean, -52.9% versus controls; P < 0.05). Topical administration of octreotide 10 microgram/day for 6 days inhibited rat cornea neovascularization induced by AgNO3/KNO3 (mean, -50.6% versus controls; P < 0.05). Octreotide 40 microgram/day i.p was tested on angiogenesis in rat mesentery obtained by i.p. injections of compound 48/80, a mast cell degranulating agent, or conditioned medium from MCF-10Aint-2 cells and was able to reduce the extent of neovascularization (mean, -45.6 and -64.1%, respectively, versus controls; P < 0.05). These data provide evidence that octreotide is an inhibitor of experimental angiogenesis in vitro and in vivo.
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PMID:Inhibition of experimental angiogenesis by the somatostatin analogue octreotide acetate (SMS 201-995). 981 82

Recent investigations support the presence of human somatostatin (SS) in the excretory system of the human lacrimal gland. To get deeper insights into a possible role of SS at the ocular surface and in the lacrimal apparatus, we investigated the distribution pattern of SS and its receptors 1-5 (SSTR1-5) by means of RT-PCR, real-time RT-PCR, Western blot and immunodot blot analysis as well as immunohistochemistry in lacrimal gland, tear fluid, conjunctiva, cornea, nasolacrimal duct epithelium, and conjunctival (HCjE) and corneal (HCE) epithelial cell lines. Cell culture experiments with HCjE and HCE were performed to analyze a possible impact of SS and inflammatory mediators on the regulation of SSTR. The results confirmed the presence of SS in lacrimal gland and tear fluid, whereas it was absent at the protein level in all other tissues and cell lines investigated. Expression of SSTR1, -2, and -5 was detectable in lacrimal gland, conjunctiva, cornea, and nasolacrimal ducts. HCjE expressed only hSSTR1 and -2, and HCE revealed only SSTR2. SSTR3 and -4 were not detected in any of the analyzed samples or cell lines. In vitro on cultured immortalized HCjE cells SS leads to a concentration-dependent down-regulation of SSTR1 mRNA but does not affect SSTR2 mRNA expression. Relative expression of SSTR1 and -2 is differentially modulated by proinflammatory cytokines and bacterial components, suggesting that the expression of both receptors is immunomodulated. Our data support an autocrine and paracrine role of SS in the lacrimal system and at the ocular surface and implicate a role of SS in corneal immunology.
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PMID:Somatostatin actions via somatostatin receptors on the ocular surface are modulated by inflammatory processes. 1910 27

Extrapituitary roles for hypothalamic neurohormones have recently become apparent and clinically relevant, based on the use of synthetic peptide analogs for the treatment of multiple conditions including cancers, pulmonary edema and myocardial infarction. In the eye, it has been suggested that some of these hormones and their receptors may be present in the ciliary body, iris, trabecular meshwork and retina, but their physiological role has yet to be elucidated. Our study intends to comprehensively demonstrate the expression of some hypothalamic neuroendocrine hormones and their receptors within different retinal and extraretinal structures of the human eye. Immunofluorescence, Western blot analysis, and RT-PCR were used to evaluate the qualitative and quantitative expression of Luteinizing Hormone Releasing Hormone (LHRH), Growth Hormone Releasing Hormone (GHRH), Thyrotropin Releasing Hormone (TRH), Gastrin Releasing Peptide (GRP) and Somatostatin as well as their respective receptors (LHRH-R, GHRH-R, TRH-R, GRP-R, SST-R1) in cadaveric human eye tissue and in paraffinized human eye tissue sections. The hypothalamic hormones LHRH, GHRH, TRH, GRP and Somatostatin and their respective receptors (LHRH-R, GHRH-R, TRH-R, GRPR/BB2 and SST-R1), were expressed in the conjunctiva, cornea, trabecular meshwork, ciliary body, lens, retina, and optic nerve.
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PMID:Expression of hypothalamic neurohormones and their receptors in the human eye. 2897 97