Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1 Prostaglandins E1 and E2 but not prostaglandin F2alpha, arachidonic acid or linolenic acid, produced slight oedema when injected into the rat hindpaw. 2 Prostaglandin E1 potentiated hindpaw oedema produced by carrageenan, kaolin, bradykinin and trypsin but not that produced by 5-hydroxytryptamine (5-HT), histamine, dextran B or compound 48/80. Carrageenan- and bradykinin-induced paw oedemas were also potentiated by prostaglandin E2. Arachidonic acid potentiated responses to carrageenan and kaolin but not responses to bradykinin, trypsin, 5-HT, histamine, dextran B or compound 48/80. Linolenic acid did not potentiate hindpaw oedema induced by carrageenan. 3 Potentiation of carrageenan-induced oedema by prostaglandin E1 was not diminished by pretreatment with indomethacin, hydrocortisone or cyproheptadine. However, arachidonic acid potentiation of carrageenan oedema was reduced by pretreatment with non-steroidal anti-inflammatory drugs but not by anti-inflammatory steroids or by paracetamol. 4 The enhancement of the response to carrageenan and kaolin by prostaglandins E1, E2 and arachidonic acid is discussed in terms of kinin mediation.
 ...
PMID:On the ability of prostaglandin E1, and arachidonic acid to modulate experimentally induced oedema in the rat paw. 118 49

The aim of this study was to determine the likely mediator(s) involved in the hypoxic-induced contraction in sheep pulmonary artery rings in vitro by studying the effects of selective receptor antagonists and enzyme inhibitors. Hypoxia caused a contraction in arteries under resting force and when precontracted with 5-hydroxytryptamine (5-HT). Flurbiprofen, a cyclooxygenase inhibitor, reduced the hypoxic contraction in 5-HT-precontracted rings but augmented the first part of the hypoxic contraction under baseline force. Inhibition of nitric oxide by haemolysate increased the hypoxic contraction under resting force. Superoxide dismutase and N-t-butyl-alpha-phenylnitrone (PBN), free radical scavenging agents, and trypsin, a proteolytic enzyme, did not produce any significant effect on hypoxia-induced constriction. Propranolol plus phentolamine, beta- and alpha-adrenoceptor antagonists respectively, did not produce any effect on hypoxic contraction under resting force, whereas these antagonists augmented hypoxic contraction in the presence of 5-HT. This combination of antagonists also caused a reduction of 5-HT contraction which was the result of alpha 2-adrenoceptor blockade. Verapamil, a calcium channel blocking drug, significantly reduced the 5-HT contraction, but did not reduce that caused by hypoxia either under resting force or in precontracted rings. These results suggest that hypoxic constriction in sheep isolated intrapulmonary artery is in part caused by reduced release of vasodilator prostanoids. This contraction does not involve voltage-operated calcium channels and is limited by release of endothelium-derived nitric oxide.
 ...
PMID:Pharmacological evidence for the role of mediators in hypoxia-induced vasoconstriction in sheep isolated intrapulmonary artery rings. 168 62

The diversity of biologically active molecules produced by vascular endothelium suggests that the endothelial cell is an active participant in numerous physiological responses, including those of the immune system. In fact, the accumulation of T lymphocytes at extralymphatic inflammatory foci represents a series of interactions between lymphocytes and vascular endothelial cells. These interactions, however, may be modulated by other factors, such as vasoactive amines. In the current study, we report that serotonin-stimulated cultured bovine aortic endothelial cells (BAECs) secrete a T-lymphocyte chemotactic cytokine (endothelial cell-derived lymphocyte chemotactic activity [ED-LCA]). Supernatants from BAECs incubated with 10(-7)-10(-4) M serotonin (5-hydroxytryptamine [5-HT]) enhanced T-cell migration, which peaked at 10(-5) M 5-HT (235 +/- 18% control migration). ED-LCA was not stored in an active form in BAECs; its secretion occurred within 60 minutes of exposure to 5-HT and was blocked by two different 5-HT2 receptor antagonists. ED-LCA was not secreted after exposure of BAECs to histamine or angiotensin II, nor was it secreted by either 5-HT-stimulated bovine pulmonary arterial or human umbilical vein endothelial cells. Physicochemical characterization of ED-LCA demonstrated that it was a trypsin-sensitive protein with an apparent molecular mass of 13-15 kDa. Preparative isoelectric focusing demonstrated pIs of 6.0 and 7.5. When applied to a molecular sieve column, the chemotactic activity corresponding to these pIs eluted in the region of 13-15 kDa. Further investigation demonstrated that partially purified ED-LCA was specific for CD4+ and CD8+ T-lymphocyte subsets and did not enhance the migration of neutrophils or monocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Restricted secretion of a T-lymphocyte chemotactic cytokine by serotonin-stimulated cultured aortic endothelial cells. 186 Jan 74

1. Sheep isolated circumflex coronary artery rings were exposed to simulated ischaemia (increased K+ reduced pH, hypoxia, reduced glucose and addition of lactate). Simulated ischaemia caused a transient relaxation lasting approximately 5 min followed by a sustained contraction that was reversible on washing with oxygenated Krebs solution. 2. Haemolysate caused a rise in baseline tension and augmented the ischaemic contraction. 3. The ischaemic contraction was abolished by BW 755C 5 microM and reduced by indomethacin 1 microM, quinacrine 50 microM or the thromboxane A2 antagonist BM 13177 10 microM. The leukotriene D4 antagonist, ICI 198615, had no effect. 4. The ischaemic-induced contraction was enhanced by propranolol 1 microM, methiothepin 1 microM and reduced by ketanserin 1 microM. 5. The ischaemic contraction was markedly inhibited by trypsin (1 mu ml-1) and by verapamil, cromakalim or sodium nitroprusside. 6. The following had no or little effect on the ischaemic contraction: Sar1-Thr8-angiotensin II, mepyramine, atropine, the spin trapping agent PBN or the free radical scavenger dimethylsulphoxide. Superoxide dismutase caused a slight enhancement. 7. The ischaemic-induced contraction was abolished by the simultaneous administration, at subthreshold concentrations, either of two vasodilators (iloprost and adenosine) or of a vasodilator and a vasoconstrictor (iloprost and U46619). 8. The ischaemic relaxation phase was reduced by propranolol and indomethacin, abolished by haemolysate and enhanced by quinacrine or cromakalim. 9. It is concluded that the ischaemic-induced contraction is caused by mediators released from the endothelium including a product of the lipoxygenase pathway. There is also evidence that simulated ischaemia causes the release of noradrenaline and 5-hydroxytryptamine.
 ...
PMID:Modification of the ischaemic-induced contraction in the sheep circumflex coronary artery by various pharmacological antagonists. 239 Jun 68

The venom of V. cincta contains acetylcholine (ACh), histamine and 5-hydroxytryptamine (5-HT). Blockers of these agonists did not block completely the hypotensive and smooth muscle contractile activity of venom. On smooth muscle, there was a residual slow contraction. The active substance which produced this slow contraction was separated by solvent extraction, gel filtration and TLC. The purified material (which has been provisionally designated "Vecikinin") lowered cat, rat and guinea pig blood pressure, increased amplitude of cardiac contraction, and increased capillary permeability. Vecikinin contracted several smooth muscle preparations (rat uterus, rat ascending colon, guinea pig ileum, guinea pig colon and rat ileum), while relaxing rat duodenum. Its contractile activity was not lost on boiling, but acid or alkali-boiling reduced its contractile activity. It was inactivated on incubation with chymotrypsin and carboxypeptidase but not with trypsin, pepsin or leucine aminopeptidase. It is a peptide, appears to be of low molecular weight, and could be distinguished from substance P, angiotensin, bradykinin and hornet or wasp kinin.
 ...
PMID:Isolation, partial purification and pharmacodynamics of a slow contractile substance in the venom sac extract of the wasp Vespa cincta Fabr. 240 29

A bland procedure, conducted in ice, is described for the extraction with HCl of smooth-muscle-contracting substances from plexus-containing ileal longitudinal muscle (l.m.) sheets obtained mainly from rabbits and some guinea-pigs. The spasmogenic activity in rabbit extracts was distinguished from acetylcholine, histamine and 5-hydroxytryptamine by antagonists; and from prostaglandins, by its insolubility in ether at acid pH and by pretreatment of the animals with indomethacin. The fact that it contracts the separated l.m. of the guinea-pig ileum, whether plexus-containing or plexus-free, and in atropine distinguishes it also from methionine-enkephalin, somatostatin, 13-norleucine motilin, bombesin, and cholecystokinin octapeptide (CCK8). This activity was partially purified, first by several partitions with ether at pH 1.4-2.2 and then by treatment at pH 4.5-5 with lead acetate. The virtual absence of ATP was confirmed by the firefly bioluminescence technique. The guinea-pig-ileum-contracting component in the partially purified extracts was destroyed by pepsin, chymotrypsin and DPCC-treated trypsin, indicating its peptide nature and distinguishing it from oxytocin, vasopressin, bradykinin, etc. In parallel assays the partially purified rabbit extracts were considerably more active than Substance P on jird or rat ascending colons than on the guinea-pig l.m., suggesting the presence of a second spasmogenic component in the extracts. In guinea-pig extracts the partially purified activity was 8-16 times greater when plexus-containing than when plexus-free, pointing to Auerbach's plexus as the source of the activity.
 ...
PMID:Extraction and partial purification of spasmogenic substances in Auerbach's plexus. 242 21

The extraction and partial purification of endogenous "monoamine oxidase (MAO) inhibitor-like" material from the monkey brain are described. The endogenous material (F-1 and F-2) obtained after Bio-Gel P-2 gel filtration and silica column chromatography inhibited MAO in the monkey brain mitochondria toward 5-hydroxytryptamine (5-HT), beta-phenylethylamine (beta-PEA), tyramine and dopamine as substrates. The inhibitory effects of F-1 and F-2 were non-linear concentration dependent, and F-1 non-competitively inhibited A-form MAO, while F-2 inhibited A-form MAO competitively and inhibited B-form MAO non-competitively. These substances were more potent inhibitors of A-form than of B-form MAO. F-2 was heat stable but liable to the treatment with pepsin and trypsin. F-1 was not inactivated by heat treatment and digestion with pepsin and trypsin. F-1 may be a low molecular weight (less than 1350) compound, including certain monoamines or their metabolites or other unidentified compounds, while F-2 was a low molecular weight (about 2500) peptide.
 ...
PMID:Endogenous monoamine oxidase inhibitor-like substances in monkey brain. 249 10

The possibility that thrombin-induced platelet reactivity could occur via both a receptor-related and a proteolytic process was examined. Thrombin elicited the formation of considerably more [32P]phosphatidic acid (an index of phospholipase C catalysed phosphoinositide metabolism) than did platelet activating factor, 5-hydroxytryptamine, ADP, and the thromboxane A2 analogue EP171, when these agents were added either alone or in combination. Co-addition of thrombin and EP171 did not evoke significantly more [32P]phosphatide acid than did thrombin alone. The protease inhibitor leupeptin, decreased but did not abolish [32P]phosphatidic acid formation elicited by either thrombin alone or thrombin in combination with EP171. The serine protease, trypsin, stimulated an increase in [32P]phosphatidic acid and this effect was additive with that of EP171. This augmentation by trypsin of EP171-induced [32P]phosphatidic acid formation was inhibited by leupeptin. These results are consistent with the concept that thrombin-induced activation of phospholipase C occurs by two distinct mechanisms: one via proteolysis, which is sensitive to leupeptin, and the other via receptor activation, a process shared by EP171. The individual components of this dual mechanism can be mimicked by the co-addition of a receptor-directed agonist (EP171) and a proteolytic agent (trypsin).
 ...
PMID:Evidence for two mechanisms of thrombin-induced platelet activation: one proteolytic, one receptor mediated. 255 47

Glucagon/PP-related peptides were detected immunohistochemically in 18 out of 22 cases of rectal tumors investigated. The reactive tumors showed prevalence of trabecular or mixed trabecular-acinar structure and moderate staining with Grimelius' silver and lead-hematoxylin. Three of the remaining 4 cases were characterized by reactivity for 5-hydroxytryptamine only, prevalence of a solid nest structural component and intense staining with Grimelius' silver technique and lead-hematoxylin. Fifteen of the 18 glucagon/PP-reactive cases were investigated immunohistochemically with a series of 6 sera directed against different sequences of glucagon, glicentin and proglucagon, and of 7 sera directed against PP, PYY and proPP-icosapeptide. A large spectrum of glucagon-related immunoreactivities, including C-terminus and mid-portion glucagon-immunoreactivity, N- and C-terminus glicentin-immunoreactivity, GLP1- and GLP2-immunoreactivity, were detected in human rectal L cells and most rectal carcinoids. With the exception of a few scattered cells in the rectal mucosa and in 3 tumors, C-terminus glucagon-immunoreactivity was obtained only after trypsin or subtilisin treatment of tissue sections. Both PYY and PP/proPP-like peptide(s) were detected in rectal L cells and carcinoids, with prevalence of PYY in normal cells and PP/proPP-like peptides in tumor cells. It is concluded that the same or closely related hormone/prohormone sequences are synthesized and stored in rectal endocrine cells and carcinoid tumors although differences of quantitative expression, post-translational cleavage or reactivity to antibodies may occur. The usefulness of protease treatments of tissue sections to unmask immunoreactivities of uncleaved propeptides or fixative-denatured peptides is outlined.
 ...
PMID:Glucagon, glicentin, proglucagon, PYY, PP and proPP-icosapeptide immunoreactivities of rectal carcinoid tumors and related non-tumor cells. 288 65

The antifibrinolytic activity was found in the medium of platelet suspension in the process of platelet aggregation induced by thrombin, ADP and 5-hydroxytryptamine. The antifibrinolytic activity was closely associated with inhibitors in platelets, which specifically inhibited plasmin activity and not inhibited other proteases such as urokinase, thrombin and trypsin. One casein unit of plasmin activity was inhibited by the inhibitors released from approximately 10(8) platelets during the aggregation with thrombin. By the activity staining analysis, it was found that there are two kinds of plasmin inhibitors with molecular weights of 25,000 and 17,000. The physiological function of these inhibitors was discussed in relation to the formation of thrombus.
 ...
PMID:Novel plasmin inhibitors released from bovine platelets during aggregation. 293 57


1 2 3 Next >>