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PubMed1986

Pepsin treatment of mammalian plasma generates immunoreactive and biologically active neurotensin-related peptides in micromolar concentrations.

Treatment of mammalian plasmas or sera with pepsin gave rise to extraordinary quantities (1-5 microM) of immunoreactive neurotensin (NT)-related peptide(s). Although immunochemical and chromatographic analyses indicated that the peptides liberated by pepsin differed from authentic neurotensin, one of the major immunoreactive products displayed NT-like biological properties. Partially purified preparations of the immunoreactive peptides increased cutaneous vascular permeability when injected intradermally in rats and released histamine from isolated rat mast cells. The pepsin-generated peptides appeared to share the biologically active C-terminal portion of NT, since they reacted with antisera selective for this region but were not recognized by N-terminal-directed antisera. Gel permeation chromatography demonstrated the presence of two substrates in plasma which liberated iNT upon treatment with pepsin, one in the albumin fraction (mol wt, 65 K) and the other a globulin (mol wt, 350 K). A variety of other proteases and substrates failed to have this effect. These results suggest the existence of a system(s) in blood, analogous to the renin-angiotensin system, for the generation of biologically active NT-related peptides.

Adult↗
PubMed2001

Pharmacological intervention with platelet phospholipase A2.

BACKGROUND: Metabolites of arachidonic acid are important regulatory substances in blood platelets. They participate in platelet adhesion and aggregation, and pharmacological intervention with arachidonate cascade is widely used in therapy of hyperactive platelets and in the prevention of thromboembolic complications. AIM OF THE STUDY: To verify and compare the effect of cationic amphiphilic drugs (CAD) from different pharmacological groups on activation of platelet phospholipase A2--the essential enzyme of arachidonic pathway in blood platelets. METHODS: Blood platelets were isolated from human and rat blood by differential centrifugation and aggregation was measured in pretreated and subsequently stimulated platelets in a dual channel aggregometer and recorded on a linear recorder. Activity of cytosolic phospholipase A2 (cPLA2) was determined by means of arachidonic acid liberation from platelet membrane phospholipids incorporated as triciated radionuclide. The radioactivity was determined by liquid scintillation method in Packard TriCarb 2500T. RESULTS: Cationic amphiphilic drugs of the beta-adrenoceptor blocking group inhibited platelet aggregation in the rank order of potency: propranolol > alprenolol > metipranolol > atenolol. Similarly did the H1-histamine antagonists bromadryl and dithiaden as well as the antimalarial chloroquine show antiplatelet effect in vitro in the rank order of potency: dithiaden > or = bromadryl > or = chloroquine. Dose-dependent inhibition of aggregation was followed by inhibition of arachidonic acid liberation from membrane phospholipids of platelets stimulated at receptor site (thrombin) or by a stimulus bypassing membrane receptors (Ca2+ ionophore A23187). The rank order potency for inhibition of stimulated 3H-AA liberation from membrane phospholipids was: a) for BAB drugs: propranolol > or = alprenolol > metipranolol, b) for other drugs: dithiaden > bromadryl > chloroquine. CONCLUSION: The drugs investigated interference with liberation of stimulated arachidonic acid showed nonspecific inhibition of platelet cytosolic phospholipase A2 by these drugs at intracellular level. The results revealed that besides inhibition of cyclooxygenase pathway, and of receptors for ADP and glycoproteins Gp IIb/IIIa, interaction of drugs with cPLA2 may represent a further site for antiplatelet action. (Fig. 5, Ref. 39.)

Adrenergic beta-Antagonists↗
PubMed1978

Biosynthesis and subcellular localization of histamine in H-110 lymphoma.

The histidine decarboxylase activity has been studied in the H-110 Lymphoma implanted in Balb-c mice. The enzymatic activity has been determined using DL-Histidine 1-14C by measuring the I--14CO2 liberated during the incubation. It has been found that the histidine decarboxylase activity in the tumor is the highest of the studied tissues. The pretreatment for 5 days with two cytostatic drugs, cyclophosphamide and 5-fluoruracile, determined a decrease of the enzymatic activity in the tumor of 33 and 54 per cent, respectively. This effect has not been observed in the lung. The pretreatment of the animals during 10 days with 0.1 mg per kg body of histamine, which in other experimental tumors induces an increase of the endogenous content of histamine, produces a decrease of the tumoral histidine decarboxylase activity. The histamine-14C uptake was not modified by this pretreatment. The subcellular localization of the radioactivity after pretreatment with histamine-14C evidenced that the nuclear fraction of the tumor contained between 2 and 10 times the radioactivity of other tissues of the same animal.

Animals↗
PubMed1987

Mechanism of histamine actions in human coronary arteries.

Helical strips of human coronary arteries contracted in response to histamine concentration dependently, they relaxed with low concentrations and contracted with high concentrations. Treatment with cimetidine potentiated contraction in the strips with intact and damaged endothelium to a similar extent and attenuated relaxation. Removal of endothelium abolished relaxation and potentiated contraction in the cimetidine-treated strips. Methylene blue increased the contractile response to histamine in the strips with endothelium but did not alter the response in the damaged-endothelium strips. Histamine-induced relaxations in the intact strips were suppressed or abolished by treatment with ETYA, AA861, a lipoxygenase inhibitor, and by chlorpheniramine but were unaffected by indomethacin. Chlorpheniramine also abolished amine-induced contraction. It may be concluded that histamine-induced contraction in human coronary arteries is mediated by H1 receptors in smooth muscle, and relaxation is mediated by H2 receptors in smooth muscle and H1 receptors in endothelium. Also, stimulation of the endothelial H1 receptor liberates vasodilator substance and possibly activates smooth muscle guanylate cyclase to accumulate cellular cyclic guanosine monophosphate.

Adult↗
PubMed1991

Histamine release during intestinal ischemia-reperfusion: role of iron ions and hydrogen peroxide.

Reactive oxygen intermediates (ROI) play a major role in the mucosal damage developing during the reperfusion period following intestinal ischemia. We have shown previously that histamine (H) release is related to the ROI generated by xanthine oxidase during intestinal ischemia-reperfusion. The present study sought to determine the possible chain of events leading to H liberation. The artery supplying a segment of the ileum was occluded for 2 hr in 51 anesthetized dogs, and plasma levels of H were determined radioenzymatically in the venous effluent. Catalase was applied to scavenge hydrogen peroxide; dimethylsulfoxide and mannitol were used as hydroxyl radical scavengers; the role of catalytically active iron was assessed by using desferrioxamine. Pretreatment with either catalase or desferrioxamine, but not with dimethyl sulfoxide or mannitol, was effective in reducing the postocclusive H release. The results provide further in vivo evidence that ROI are causative agents in H liberation during reperfusion of the ischemic gut. Hydrogen peroxide can interact with catalytically active iron and generate highly reactive oxidants, which in turn are responsible for H release. The exact nature of these oxidants is still uncertain.

Animals↗
PubMed1985

[Functional morphology of stomach secretions].

The stimulation of gastric secretion is regulated by neurovagal, endocrine and immunological reactions. During the gastric phase of digestion, especially acetylcholin, gastrin and histamin react as main transmitters, activated by mediators (prostaglandines, leucotrienes, lipoxygenases). The dominant role of nervus vagus has to be seen in the transactions of vago-vagal reflexes, the stimulation of gastrin liberation by an non-cholinergic mechanism and the regulation of the gastric microcirculation. The antrum pylori can be seen as an immunological area of reception, where immunological active cells (macrophages, NK-lymphocytes and T-lymphocytes) are recognizing antigens (e.g. food antigens). These immunocytes induce a cascade of endocrine and exocrine mechanisms of digestion. Mastcells, located intra-and extraepithelial, take a regulatory influence in producing histamins, leucotrienes and also prostaglandines.

Animals↗
PubMed1991

In vitro ketotifen protection in bronchial hyperreactivity.

There are drugs, such as ketotifen, that inhibit bronchospasm through different mechanisms. In this study, we looked at the changes in the number of sanguineous cells that ketotifen produces, especially in basophil cells, that could explain its prophylactic effects in bronchial hyperreactivity disclosed by exercise, as well as its relation to the variations in basal and total histamine in blood. 22 patients were selected, with a diagnosis of extrinsic bronchial asthma with sensitization against Dermatophagoides, and were compared to a control group. They all underwent an exercise test. Blood samples were taken before and after exercise in order to measure the number of leukocytes and the changes in basal and total histamine. We found that the number of basophils does not increase after exercise in untreated patients, while it does in the control group and in treated patients. This implies that ketotifen stabilizes the basophil cells, hindering their degranulation and the subsequent liberation of mediators that would produce bronchospasm after exercise.

Adolescent↗
PubMed1962

Dual action of nitroparaffins on the guinea-pig ileum.

Nitroparaffins act on the guinea-pig ileum by several mechanisms. They produce contraction partly by ganglionic stimulation and partly by direct liberation of transmitter from the nerve endings. They also inhibit the response to acetylcholine and nicotine, but interfere less with the action of histamine, serotonin or bradykinin. The two opposite effects of the nitro compounds are independent of each other. Within the homologous series of normal nitroparaffins, the excitatory action diminishes and the inhibitory effect increases with the lengthening of the carbon chain.

Acetylcholine↗
PubMedDate not supplied

Regulatory mast cells. I Suppressive action of their products on an in vitro primary immune reaction.

Products of mast cell degranulation, as well as histamine and serotonin, were added to a Mishell and Dutton preparation for in vitro primary immunisation (induction of IgM antibody formation) to sheep or horse red blood cells. Degranulation products were either obatined beforehand by reacting passively sensitised mast cells with the corresponding antigen (unrelated to or identical with the in vitro immunising antigen) or liberated into the culture medium where mast cells actively sensitised to the in vitro immunising antigen had been added. A 46 to 72 % reduction of direct (IgM) plaque forming cells was observed in all cases. This reduction was prevented by anti-histamine. The responsible mediators were active in the 0 to 24 hour period after antigen introduction. The anaphylactic degranulating antibodies triggering this inhibitory activity were found to be thermolabile in one experiment. An in vivo-induced mast cell degranulation led to a reduced formation of plaque forming cells. The enhancing and immunoregulatory activity of anaphylactic mouse antibodies is therefore tentatively and at least partially attributed to their capacity to degranulate mast cells after contact with the antigen.

Animals↗
PubMed1988

Xenopsin-related peptide generated in avian gastric extracts.

Two avian counterparts to amphibian xenopsin have been identified as H-Phe-His-Pro-Lys-Arg-Pro-Trp-Ile-Leu-OH (XP-2) and its partial sequence H-His-Pro-Lys-Arg-Pro-Trp-Ile-Leu-OH (XP-1) isolated from extracts of turkey proventriculus and skin. Both peptides were shown to be present within these and other tissues primarily (99%) in precursor form(s), from which they were liberated by the action of endogenous enzyme(s) during extraction. Synthetic and native preparations of XP-2 increased vascular permeability in rats and released histamine from isolated rat mast cells at submicromolar concentrations. The ubiquitous distribution of this XP-related sequence and its pharmacologic capabilities suggest potential roles in the general regulation of tissue blood flow and fluid exchange.

Amino Acid Sequence↗
PubMed2007

The effect of n-3 PUFA on eNOS activity and expression in Ea hy 926 cells.

The aim of this study was to evaluate the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on NO synthase (eNOS) activation in Ea hy 926 endothelial cells. EPA or DHA (0-80 microM), added to the culture medium during 24h, were dose-dependently incorporated into the cells. In control medium, eNOS activity (evaluated by the citrulline assay) and eNOS phosphorylation on Ser 1177 were correlated. They were increased by 10 microM histamine and prevented by 20 microM lysophosphatidylcholine (LPC). By contrast, EPA or DHA increased basal phosphorylation without affecting eNOS activity in non-stimulated cells, but dose-dependently decreased this activity in histamine-stimulated cells without modifying the phosphorylation level. Furthermore, EPA and DHA did not prevent the deleterious effects of LPC on histamine stimulation. In conclusion, incorporation of EPA and DHA could be deleterious for endothelial cells by deregulating the activation of eNOS and preventing NO liberation.

Blotting, Western↗
PubMed1997

The H1-histamine antagonist dithiaden inhibits human platelet function in vitro.

The H-histamine receptor antagonist Dithaden inhibited in a dose-dependent manner, human platelet 1 aggregation in vitro that was induced with stimuli in the following rank order of potency: thrombin > A23187 > adrenaline > ADP. The aggregation of platelets in plasma induced with adrenaline was inhibited by Dithiaden (DIT) (both the first and the second phase) and the onset of the second phase was prolonged significantly. In a concentration-dependent manner DIT inhibited thrombin- and calcium ionophore A23187-induced {3H}arachidonic acid liberation from, and peroxidation (measured as malondialdehyde formation) of membrane phospholipids. The same effect of DIT was found for the inhibition of thromboxane B suggested that DIT does not inhibit stimulated platelets at specific histamine receptors sites but rather at the phospholipase A and thromboxane synthase level. Results from in vitro experiments should be verified in 2 vivo . generation. It is 2.

Journal Article↗
PubMedDate not supplied

[Study of histamine in asthma].

Histamine is generally considered as the principal chemical mediator in experimental allergy of type I and anaphylaxis. However, its part in human bronchial asthma remains discussed, because neither the dosage of histamine in blood, nor the use of antihistaminics have furnished any real evidence. This study is dealing with two elements: the importance of local bronchopulmonary phenomena, and the associated mediators also liberated in asthma, such as SRSA. ECFA, kinines, prostaglandins and disorders of balance between, on one hand, alpha and beta-actions of the catecholamines, and on the other hand, between the two main types of cyclic nucleotides. These considerations should allow a better approach of the asthma etiopathology and perhaps an improvement of its treatment.

Animals↗