Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A detailed review of the hormonal effects on intraocular pressure is presented. There is evidence that corticotropin, vasopressin, thyroxin, insulin, glucocorticoids and mineralocorticoids may play a role in the physiologic regulation of intraocular pressure. Growth hormone, melanocyte stimulating hormone, progesterone, estrogen, chorionic gonadotropin and relaxin may influence intraocular pressure when administered in pharmacologic doses. Whether the key to understanding primary open-angle glaucoma lies in recognizing abnormal endocrine mechanisms, especially involving glucocorticoids, remains unclear at the present time.
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PMID:Hormonal regulation of intraocular pressure. 41 3

The aqueous flare (AF) of an intact rabbit eye was measured by a photoelectrical instrument and the intraocular pressure by vibration tonometry. Prior treatment with imidazole given intraperitoneally noticeably inhibited the disruption of the blood-aqueous barrier in rabbit eyes induced by topical prostaglandin E2 (PGE)2, topical arachidonic acid (AA), infrared irradiation of the iris, endotoxin of Proteus mirabilis given intravenously, and alpha-melanocyte-stimulating hormone (alpha-MSH) given subcutaneously. Prior treatment with imidazole given topically had no effect on the disruption of the blood aqueous barrier caused by topical PGE2, topical AA, infrared irradiation of the iris, or endotoxin of P. mirabilis given intravenously, but facilitated and potentiated strongly the response to alpha-MSH given subcutaneously. Prior treatment with topical imidazole did not affect the histological changes of the anterior ciliary processes induced by alpha-MSH given subcutaneously.
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PMID:The effect of imidazole on the disruption of the blood-aqueous barrier in the rabbit eye. 77 Mar 85

The effects of somatostatin, cyclo(D-Trp-Lys-Thr-Phe-Pro-Phe) acetate, a somatostatin analog, neurotensin, and met-enkephalin were studied in the rabbit eye by measuring the intraocular pressure (IOP), aqueous humor protein concentration, ocular blood flow and the pupil diameter. Somatostatin or the analog injected intracamerally (10 micrograms/eye) and infused intra-arterially (0.6-4 micrograms/min) had no significant effect on the parameters studied in normal eyes. However, somatostatin and, particularly, the analog attenuated the miotic response to a standard nociceptive stimulus consisting of topical application of 1% neutral formaldehyde. The other component parts of the irritative response were not attenuated. Intracameral injection of 1-2 micrograms neurotensin caused vasodilation in the anterior segment of the eye, a slight increase in aqueous humor protein concentration, and some decrease in IOP. Intracameral injection of 1-50 micrograms met-enkephalin had no effect on the blood-aqueous barrier, IOP or the pupil diameter. Neither did this dose of met-enkephalin attenuate the miotic response to exogenous substance P. It seems likely that somatostatin and the somatostatin analog attenuate the miotic response to nociceptive stimuli by preventing the release of a substance, presumably substance P, from sensory nerves.
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PMID:Effects of somatostatin, a somatostatin analog, neurotensin and met-enkephalin in the eye with special reference to the irritative response. 290 80

The effects of intracameral (i.c.) administration of MIF-I on the ocular response to alpha-MSH were tested in rabbits. In confirmation of previous studies, i.c. alpha-MSH significantly increased intraocular pressure (IOP) and reduced pupillary diameter (PD). Concomitant administration of alpha-MSH and MIF-I antagonized both the IOP increase and miosis induced by alpha-MSH. Aqueous humor (AH) dynamics studies revealed that alpha-MSH increases IOP, possibly, by decreasing AH outflow. The decreased AH outflow induced by alpha-MSH was antagonized by concurrent administration of MIF-I and alpha-MSH. MIF-I did not affect IOP or PD when administered alone. These results add more support for a role of alpha-MSH in ocular function, and suggest that the ocular response to alpha-MSH may be subject to inhibitory control by MIF-I.
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PMID:Inhibition by MIF-I of alpha-MSH induced increase of intraocular pressure and miosis in rabbits. 290 21

A growing body of evidence suggests that neural peptides may induce important modulations on vegative and motor functions of the eye. The present study was designed to evaluate the effect of intracameral (I.C.) administration of alpha-melanocyte-stimulating hormone (alpha-MSH) and several other ocular peptides on intraocular pressure (IOP) in rabbits. alpha-MSH (5 micrograms) produced a significant and prolonged unilateral increase of IOP. This effect of I.C. alpha-MSH was dose-dependent (ED50 = 2.5 micrograms). Structure-activity studies revealed that equimolar doses of beta-MSH and gamma-MSH, unlike alpha-MSH, were totally ineffective. In addition, the structurally unrelated peptides beta-endorphin, thyrotropin-releasing hormone (TRH) and gonadotropin-releasing hormone (Gn-RH) did not affect IOP, when tested in a dose equimolar to 5 micrograms of alpha-MSH. These results confirm and extend previous observations, suggesting that alpha-MSH may be an important factor involved in regulation of IOP.
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PMID:Intracameral administration of alpha-MSH increases intraocular pressure in rabbits. 408 Jan 14

The present investigation was designed to evaluate the effect of selected peptides on pupillary diameter and intraocular pressure (IOP) in rabbits. Intracameral (IC) administration of neurotensin (NT) in doses of 5-100 micrograms produced a significant, long lasting and dose-dependent decrease in pupillary diameter without affecting IOP. NT-induced miosis appears to be relatively specific because a variety of peptides including Gn-RH, somatostatin, met-enkephalin, bombesin, leu-enkephalin or NT1-6, (a biologically inactive N-terminal fragment of NT), produced no effect on pupillary diameter; only substance P produced miosis similar to NT when tested in a dose equimolar to 30 micrograms of NT. In addition, peripheral (intravenous) administration of NT (100 micrograms/kg) was equally ineffective. Inhibition of prostaglandin synthesis with indomethacin, did not prevent subsequent NT-induced miosis. Finally, IC administration of an effective dose of NT (30 micrograms) did not alter the protein concentration in the aqueous humor. These results indicate that NT-induced miosis is not mediated by endogenous prostaglandins and that this effect of NT does not appear to involve disruption of the blood-aqueous barrier, suggesting that NT may play a role in regulation of pupillary diameter.
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PMID:Intracameral administration of neurotensin induces miosis in the rabbit. 619 87

The aim of the study was to determine if early steroid treatment of infantile spasms is associated with ocular complications years after its termination. Twenty-five patients with infantile spasms who underwent prolonged treatment with intramuscular synthetic adrenocorticotropic hormone (ACTH) and oral prednisone were evaluated for ocular complications 2 to 33 years after treatment cessation. Patients were followed by an ophthalmic examination that included anterior and posterior segments and measurement of intraocular pressure. Intraocular pressure was normal bilaterally in all patients. Findings on anterior segment examination were unremarkable. On posterior segment examination, 3 patients had an increased cup/disc ratio with normal intraocular pressure. In 2 patients, the increased ratio was considered an anatomical variant. Posterior segment findings in 2 patients were attributed to their background disease. In conclusion, early treatment with high-dose synthetic adrenocorticotropic hormone and oral prednisone for infantile spasm is apparently not associated with a risk of occular complications on long-term follow-up.
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PMID:Long-term follow-up for ophthalmologic sequelae in children treated with corticosteroids for infantile spasms. 2211 11