Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied, using anesthetized albino rabbits, whether polymodal receptors are responsible for rise in the intraocular pressure (IOP) caused by algesic substances, and also whether substance P (SP) is involved in this phenomenon. Intracameral administration of bradykinin (BK), SP, hypertonic saline, and hypertonic glucose caused an IOP rise. The IOP responses to BK and hypertonic saline were reduced by benoxinate, but aspirin reduced only the response to BK. Repeated applications of BK caused a decrease in subsequent responses (tachyphylaxis). These results are consistent with the characteristics of responses of polymodal receptors, and suggest that these IOP responses are produced by neurogenic inflammation. The IOP response to SP also showed tachyphylaxis, but after the tachyphylaxis to SP had been established, subsequent intracameral administration of BK still produced a marked rise in IOP. Moreover, the administration of SP into the posterior chamber, which is known to be the site of the blood-aqueous barrier, caused a much smaller rise in the IOP. These observations indicate that the IOP response to algesic substances might be caused by activation of the polymodal receptors, and that SP might not be a mediator in these responses.
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PMID:Implication of polymodal receptor activities in intraocular pressure elevation by neurogenic inflammation. 169 16

The effects of ruthenium red, an inorganic dye with known capsaicin antagonist properties, was investigated in the rabbit eye. At a dose of 0.24 nmol ruthenium red inhibited the inflammatory effects of capsaicin (1 or 8 nmol). Unexpectedly, when the dye was injected in doses ranging from 0.24 to 7.4 nmol, it caused an inflammatory response with constriction of the pupil (miosis) and a breakdown of the blood-aqueous barrier, leading to a rise intraocular pressure. Tetrodotoxin (30 nmol) inhibited the ruthenium red-induced rise in intraocular pressure but had less effect on the miotic response. The tachykinin antagonist spantide inhibited the miosis but had no effect on the rise in intraocular pressure. Ruthenium red induced an increase in substance P-like immunoreactivity and calcitonin gene-related peptide-like immunoreactivity in the aqueous humor. These levels were positively correlated with the rise in aqueous humor protein concentration. The ruthenium red-induced miosis and, to a less extent, the rise in intraocular pressure were inhibited by the Ca2+ channel-blocking agent omega-conotoxin GVIA (CTX), indicating a partial dependence on an influx of extracellular Ca2+. CTX also attenuated the miotic effect of capsaicin but had no effect on the capsaicin-induced rise in intraocular pressure. It is concluded that, in the rabbit eye, ruthenium red induces a neurogenic inflammatory response besides its capsaicin antagonist effects.
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PMID:Ruthenium red and capsaicin induce a neurogenic inflammatory response in the rabbit eye: effects of omega-conotoxin GVIA and tetrodotoxin. 172 55

This lecture summarizes studies on the effects of some of the neuropeptides which seem to be present in somatosensory and autonomic nerves in the uvea. Release of these peptides is likely to explain nerve induced effects in the eye which are not due to classical transmitters. Trigeminal nerve fibres in the eye seem to contain substance P (SP), calcitonin gene-related peptide (CGRP), and cholecystokinin (CCK), parasympathetic nerve fibers from the facial nerve seem to contain vasoactive intestinal polypeptide (VIP), and peptide with histidine and isoleucine terminals (PHI), and sympathetic nerves seem to contain neuropeptide Y (NPY). Retrograde trigeminal nerve stimulation in rabbits causes hyperemia, miosis, a breakdown of the blood-aqueous barrier to plasma proteins and a rise in intraocular pressure (IOP). There is release of SP and CGRP or related peptides. The miosis seems to be due to SP and the other effects to CGRP and small amounts of arachidonic acid metabolites released by the peptides. SP has no miotic effect in monkeys and cats. However, CCK is a potent miotic in monkeys and causes contraction of the human pupillary sphincter muscle. It has no such effect in the lower species. The effect of CCK in primates seems to derive from the presence of CCK receptors of the A-type on the pupillary sphincter muscle, and can be blocked by lorglumide. Miosis can be produced in cats by the peptide endothelin; this effect is due to release of arachidonic acid metabolites. Facial nerve stimulation causes vasodilation in the uvea of rabbits, cats and monkeys. The effect cannot be abolished by muscarinic blocking agents.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The 1990 Endre Balazs Lecture. Effects of some neuropeptides on the uvea. 187

The structure of the anterior segment of the eye provide aqueous humour for metabolic traffic, regulation of intraocular pressure and the maintenance of a functional permeability barrier to separate internal compartments from general systemic influences. Irritative and injurous insults to the eye elicit an acute defensive miotic and vascular response which upsets the aqueous dynamics and provokes the influx of blood plasma proteins into the aqueous chambers. These events are initiated by antidromic activation of sensory elements within the anterior segment, releasing substance P and calcitonin gene-related peptide (CGRP) which, in lower mammals at least, stimulate respectively the miotic and vascular reactions. Considerable species differences can be found in the responsiveness of the eye to injury and in the effects of exogenous CGRP and substance P.
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PMID:Review: mediation of the ocular response to injury. 209 17

The irritative response to Nd:YAG laser capsulotomy was studied in unanaesthetized rabbits. Posterior lens capsulotomy with a total energy of 100 mJ had no effect on the pupil size but increased the intraocular pressure by 5-10 mmHg and caused a breakdown of the blood-aqueous barrier. Anterior lens capsulotomy with a total energy of 20, 60 or 100 mJ caused constriction of the pupil, and an increase in intraocular pressure in a dose-dependent manner, and a breakdown of the blood-aqueous barrier. Indomethacin attenuated all the component parts of the irritative response and (D-arg1, D-pro2, D-trp7,9, leu11)-SP attenuated the miotic response. A combination of indomethacin and the substance P antagonist almost completely abolished the irritative response. This indicates that the acute YAG-laser-induced irritation in the rabbit eye is dependent both on a release of prostaglandins and on substance P, the former probably releasing the latter from sensory nerves.
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PMID:A study of the mechanism of ocular irritation following YAG laser capsulotomy in rabbits. 243 20

Calcitonin gene-related peptide (CGRP) in the anterior uvea coexists with tachykinins (substance P and neurokinin A) in sensory nerve fibers deriving from the trigeminal ganglion. Mechanical or electrical stimulation of the intracranial part of the trigeminal nerve/ganglion in rabbits produced a marked hyperemia in the anterior segment of the eye, increased intraocular pressure, breakdown of the blood-aqueous barrier and miosis. Simultaneously, CGRP-like immunoreactivity was released into the aqueous humor. This suggests that the highly vasoactive CGRP can be released from sensory nerve fibers to participate in vascular responses. Unlike the tachykinins, CGRP per se was without effect on the pupillary diameter while disrupting the blood-aqueous barrier (resulting in aqueous flare) upon intravitreal injection. In addition, CGRP enhanced the aqueous flare evoked by a minimal eye trauma (infrared irradiation of the iris). The miosis evoked by the intravitreal injection of substance P was more pronounced when CGRP was injected simultaneously, and finally, substance P induced aqueous flare much more effectively when given together with a threshold dose of CGRP.
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PMID:Calcitonin gene-related peptide in the eye: release by sensory nerve stimulation and effects associated with neurogenic inflammation. 243 15

The effects of calcitonin gene-related peptide (CGRP) and substance P (SP) on the regional blood flow of the eye were studied in cats. The animals were anaesthetized and the eyes were cannulated for intracameral administration of the test substances and intraocular pressure measurement. Regional blood flow was determined using the radioactively labelled microsphere method. Intracameral injection of 1.3 x 10(-9) mol of CGRP increased markedly the blood flow of the iris, the ciliary body, and the sclera. There was no clear-cut effect in the choroid or in the retina. Intracameral administration of 1.3 x 10(-9) mol of SP had no clear-cut effect on the blood flow of any of the ocular tissues studied. In addition, CGRP reduced the intraocular pressure statistically significantly, whereas SP had no effect. The results of the present study indicate that CGRP is a potent vasodilator in the anterior uvea of the cat eye when administered from the adventitial side, whereas SP seems to have little or no effect.
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PMID:Effects of calcitonin gene-related peptide and substance P on regional blood flow in the cat eye. 245 7

The effect of intracameral injection of 1.0 micrograms of substance P (SP) on the regional ocular blood flow in albino rabbits was investigated by a method using radioactively labelled microspheres. The mean ciliary blood flow in SP-treated eyes was 0.163 +/- 0.006 g/min and in the control eyes 0.107 +/- 0.004 g/min. The flow increase was 72 +/- 22%. The mean difference was 0.056 +/- 0.005 g/min (P less than 0.01, n = 11). Infusion of 25-40 micrograms of substance P into one common carotid artery over 20-45 min caused a rise in intraocular pressure of 22.5 +/- 1.5 cm H2O in the ipsilateral eye and of 1.6 +/- 0.2 cm H2O in the contralateral one. The mean difference was 19 +/- 5.3 cm H2O (P less than 0.05, n = 4). The protein concentration of the aqueous humour on the ipsilateral side was higher than on the contralateral one, and there was marked extravasation of intravenously injected Evans blue in the ciliary processes in the ipsilateral eyes. Extravasation of Evans blue int he ciliary processes and a rise in intraocular pressure also occurred in two rabbits which were given in intravenous injection of SP (0.37 or 3.4 mg). It is concluded that in rabbits SP tends to increase the intraocular pressure and to cause a breakdown of the blood-aqueous barrier and that the increase in ciliary blood flow caused by SP may play a role in these mechanisms.
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PMID:Effects of substance P on regional ocular blood flow, intraocular pressure and blood-aqueous barrier in rabbits. 247 86

This study was undertaken to characterize the mechanism of ocular irritation to YAG laser capsulotomy in rabbits. The blocking agents were administered intravitreally. (D-Arg1,D-Pro2,D-Trp7,9)-SP, a substance P antagonist, tended to reduce miosis but had no effect on intraocular pressure (IOP). It had less effect on miosis than (D-Arg1,D-Pro2,D-Trp7,9,Leu11)-SP another SP antagonist. Met-enkephalin and tetracaine had no effect on miosis or the increase in IOP after YAG laser capsulotomy, whereas tetrodotoxin reduced miosis, but had no clear-cut effect on IOP, or the increase in aqueous humor protein concentration. This indicates an involvement of sensory neurons with release of SP or a closely related peptide in the miotic component part while the increase in IOP and the barrier breakdown probably are dependent mainly on a release of prostaglandins.
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PMID:Characterization of the mechanism of acute ocular irritation to YAG laser capsulotomy in rabbits: effects of substance P antagonists, Met-enkephalin, tetracaine and tetrodotoxin. 248 Dec 50

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


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