Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acid-acetone extracts of the chicken rectum were subjected to chromatographic and electrophoretic separation, and two new smooth muscle-contracting substances close to purity were obtained. One of them showed chemical and biological characteristics similar to those of substance P, but it was clearly different from substance P on the basis of chromatographic and electrophoretic criteria. Thus, one could be a peptide belonging to the substance P-family. The other substance was also shown to be of peptide nature since its biological activity was destroyed by chymotrypsin and carboxypeptidase A. Parallel bioassay on the two tissues of the longitudinal muscle of the guinea-pig ileum and the isolated whole chick rectum revealed that none of the peptides such as substance P, physalaemin, kassinin, eledoisin, bradykinin and angiotensin II could be a candidate for the active substance. The biological activity was not antagonized by naloxone, suggesting that the substance was a peptide other than the opioid compounds. The molecular sizes estimated by gel filtration are 1300 for the substance P-like peptide and 1600 for the other substance. The possible physiological roles of the two substances as an excitatory non-adrenergic, non-cholinergic transmitter were discussed.
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PMID:Isolation of smooth muscle excitatory substances from chicken rectum and their characterization. 395 45

We have tested the effects of intravenous injections of substance P (SP), bradykinin (BK), somatostatin (SS) and vasoactive intestinal peptide (VIP) on the blood pressure, histaminemia and hematocrit in pentobarbital-anesthetized rats. The four peptides elicited a decrease of the mean arterial blood pressure which varied both in amplitude and in duration depending both on the peptide and on the doses utilized. The hypotensive effects of SP and VIP were more persistent than those caused by BK or SS. Only SP evoked an increase of histaminemia. Both SP and BK caused an increase of hematocrit. The change of hematocrit was more prominent and of longer duration after Sp than after BK. Pretreatment of rats with the antiinflammatory drug dexamethasone inhibited markedly the changes of blood pressure, histaminemia and hematocrit caused by SP. The hypotensive effects of BK, SS and VIP as well as the transient change of hematocrit evoked by BK were not affected by dexamethasone. The results suggest that part of the hypotensive activity and changes of hematocrit evoked by SP in rats is due to the release and action of histamine and possibly of other vasoactive substances, of mast cell origin. The results also indicate that mast cell mediators, particularly histamine, are unlikely to be instrumental in the hypotensive activity of BK, SS or VIP in rats.
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PMID:Evaluation of the contribution of mast cell mediators to the hypotensive activity of various peptides in rats. 619 Dec 39

Histamine secretion was induced by substance P, in a dose-dependent manner, from rat peritoneal mast cells, both in the presence and absence of Ca2+ in the medium, and disodium cromoglycate (DSCG) produced a dose-dependent inhibition of the histamine secretion in Ca2+-containing medium. However, in the absence of Ca2+, DSCG was ineffective or had a far weaker activity. Mg2+, Sr2+ and Ba2+ were ineffective in restoring the DSCG activity when added to medium devoid of divalent metal ions. Therefore, extracellular Ca2+ seems to be a specific requirement for the binding of DSCG to its "receptors" on the mast cell surface or some steps in the DSCG action.
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PMID:Disodium cromoglycate inhibition of substance P-induced histamine secretion is calcium dependent. 619 41

The mechanism of selective, non-immunological histamine release from mast cells, caused by various endogenous substances, is not clearly understood. Since in vivo experiments indicate that the local control of secretory cells is influenced by acetylcholine and peptides, we investigated whether the secretion of histamine is similarly regulated in the mast cell. Experiments were performed with peritoneal cavity cell suspensions (PCS) of the rat. The endogenous polypeptide substance P, compound 48/80 and a non-hydrolysable cholinomimetic agonist, carbachol, were used. The concentrations of the drugs were kept low to avoid non-specific histamine release caused by morphological damage of mast cells. It was found that: (1) carbachol (2 X 10(-5) M) did not release histamine from PCS, (2) substance P (6.5 X 10(-6) M) released histamine and this effect was increased by the addition of carbachol (2 X 10(-5) M); the effect of carbachol was inhibited by atropine , (3) carbachol (2 X 10(-5)M) did not increase histamine release caused by compound 48/80 (0.02 micrograms/ml). From these experiments it may be concluded that activation of peptidergic receptor(s) can cause histamine release from mast cells and that muscarinic agents may be involved in the regulation of the(se) receptor(s).
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PMID:The interaction of cholinomimetics, peptides and compounds 48/80 on histamine secretion from the mast cell. 620 51

Characteristics of histamine (Hi) and 5-hydroxytryptamine (5-HT) release from rat peritoneal mast cells in response to the polypeptide adrenocorticotropin (ACTH) were studied. During a 15 min incubation at 37 degrees C, ACTH evoked Hi as well as 5-HT release from rat mast cells at concentrations of 1 X 10(-4) M-1 X 10(-3) M. The release was dose-dependent and very rapid. After 15 sec the amount of the amines released was the same as after 4.5 min. In most experiments, the percentage of Hi release was slightly but significantly higher than the percentage of 5-HT release. Hi and 5-HT release induced by ACTH also took place in a calcium-free medium. However, the release of the amines was decreased when calcium was omitted. Comparison of the effects of ACTH, compound 48/80 and substance P on mast cell secretion showed that ACTH is about 100 times less active then substance P which was in turn about 100 times less active than compound 48/80. When both ACTH and compound 48/80 were used together as liberators , the release was significantly higher than with either liberator alone. Our results indicate that there are receptor sites for the endogenous polypeptide ACTH on the mast cell membrane which mediate Hi and 5-HT release. This release was found to resemble that evoked by the basic secretogogue compound 48/80 but in some aspects to be different from that evoked by substance P.
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PMID:The effect of adrenocorticotropin on histamine and 5-hydroxytryptamine secretion from rat mast cells. 620 67

Increasing concentrations of neurotensin produced a biphasic contractile response, inhibition followed by excitation, when added to full-thickness circular strips of canine gastric corpus muscle cut in a circular orientation and incubated at 37 degrees C in vitro. The inhibitory response (mean effective concentration (EC50) 7 x 10(-9)M) was not altered by addition of concentrations of tetrodotoxin or scorpion venom sufficient to block field-stimulated neural responses nor by any other antagonist tested. Therefore, it would appear that inhibition is due to an excitation of the smooth muscle receptor. The excitatory response (EC50 4 x 10(-7)M) was only present in full-thickness strips, i.e., was absent in strips of circular muscle, and was reduced by mepyramine or histamine tachyphylaxis. Pretreatment with disodium cromoglycate or repeated doses of 48/80 to extinction of the response completely eliminated the excitatory response as did repeated doses of substance P to tachyphylaxis. Since 48/80 and substance P have been shown to degranulate mast cells and disodium cromoglycate to stabilize mast cell membranes, neurotensin would appear to produce excitation by releasing histamine and other material from mast cells. In contrast to in vivo studies, where two classes of receptors producing inhibition were found, i.e., a high-affinity receptor on adrenergic nerves and a lower affinity receptor on smooth muscles, in vitro there appears to be only one class of receptor producing inhibition on the smooth muscle itself as no neural receptors were found. The neurotensin receptor responsible for excitation appeared to be on mast cells. The action of neurotensin thus depends upon the locus and the affinity of the receptor and the presence of the receptor on the method of study, i.e., in vivo vs. in vitro.
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PMID:Mechanisms of action of neurotensin on motility of canine gastric corpus in vitro. 683 7

The pharmacology of the early and delayed phases of the neurogenic oedema responses to electrical stimulation of the saphenous nerve was studied in anesthetized rats using a quantitative Evans blue dye leakage technique. The immediate response to 5 min nerve stimulation was not reduced by aprotinin or mepyramine in combination with methysergide. However the response measured 10 min later and also that to 15 min nerve stimulation were reduced by these agents indicating that kinins and mast cell amines might be released after some delay, but they did not contribute significantly to the early phase of the response. Results with indomethacin indicated that prostaglandins were not involved in the later phase of the response. Bacitracin which has been reported to potentiate the sialogogic effect of substance P, the most likely candidate for primary mediator of neurogenic oedema, was without effect on the early phase of the response. Morphine, which has been suggested to inhibit stimulus-evoked substance P release from primary afferent terminals, reduced the early phase of the neurogenic oedema response but it also reduced blood pressure. Both effects were abolished by naloxone and thus it is likely that the reduction in the neurogenic oedema response was due to the depressor action of morphine. In confirmation of previous findings, capsaicin pretreatment of both adult rats and rats as neonates resulted in marked reduction of the neurogenic oedema response without effect on the vascular permeability response to substance P.
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PMID:Pharmacology of the neurogenic oedema response to electrical stimulation of the saphenous nerve in the rat. 723 72

Evidence is provided here supporting the existence of a novel autacoid mechanism negatively modulating mast cell behaviour in response to noxious stimuli in vivo; hence, the denomination "autacoid local inflammation antagonism" (ALIA). In particular, as lipid amides of the N-acylethanolamine type have been reported to accumulate in tissues in degenerative inflammatory conditions, we examined whether these N-acylated lipids could exert regulatory effects on mast cell activation in vivo. The results reported show that both long- and short-chain N-acylethanolamines, when systemically administered, are effective in reducing mast cell degranulation induced by local injection of substance P in the ear pinna of developing rats. These and other data suggest that the endogenous production of N-acylethanolamines may constitute a local autocrine/paracrine response for the negative feedback control of mast cell responses to various activating signals. Such a process may be of physio-pathological relevance in the regulation of functional neuro-immune-mast cell interactions.
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PMID:A proposed autacoid mechanism controlling mastocyte behaviour. 750 99

Substance P (SP), neurokinin A (NKA) and calcitonin gene-related peptide (CGRP) coexist in nerve fibres in the skin. CGRP causes erythema upon intracutaneous injection. The erythema is independent of axon reflexes and release of mast cell histamine. SP is known to produce a flare reaction that is dependent on axon reflexes and release of mast cell histamine. The flare reaction to NKA is known to depend predominantly on axon reflexes. The purpose of the present study was to investigate possible cooperation between SP and CGRP. SP was found to shorten the duration of the reddening induced by CGRP, injected concomitantly. NKA did not shorten the duration of the CGRP response. Local elimination of mast cells in the skin by treatment with compound 48/80 had the effect that SP lost its ability to shorten CGRP-evoked erythema. These observations support the suggestion that an SP-evoked release of proteolytic enzymes from mast cells could lead to accelerated degradation of CGRP.
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PMID:Interaction between tachykinins and CGRP in human skin. 750 67

Norathyriol, a xanthone aglycon isolated from Tripterospermum lanceolatum, was demonstrated to reduce the plasma leakage elicited by the passive cutaneous anaphylactic reaction in normal as well as in adrenalectomized mice. Capsaicin pretreatment greatly suppressed the local edema caused by antidromic stimulation of the saphenous nerve. The plasma exudation of neurogenic inflammation was also reduced in mice treated with norathyriol, diphenhydramine and methysergide, but not with indomethacin. Norathyriol, cyproheptadine and diphenhydramine combined with methysergide suppressed the ear edema caused by injection of compound 48/80, bradykinin and substance P into the ear. However, indomethacin did not affect this phlogist-induced edema response. Histamine- and serotonin-induced plasma exudation in ear edema was also reduced by norathyriol. In isolated rat peritoneal mast cell preparations, norathyriol produced a dose-dependent inhibition of histamine and beta-glucuronidase release from mast cells challenged by compound 48/80, bradykinin and substance P. In compound 48/80-pretreated mice, norathyriol at higher concentrations suppressed the bradykinin- and substance P-induced ear edema to a significantly greater extent than diphenhydramine combined with methysergide did. These data indicate that the inhibitory effect of norathyriol on local edema is not due to the release of steroid hormones from the adrenal gland, but is probably partly due to suppression of mast cell degranulation and hence reduce the release of chemical mediators which increase vascular permeability, and partly, at least in higher doses, due to protection of the vasculature from challenge by various mediators.
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PMID:Inhibitory effect of norathyriol, a xanthone from Tripterospermum lanceolatum, on cutaneous plasma extravasation. 751 Nov 7


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