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Biomedical subjects

G B West

Publications and source records attributed to G B West.

At least 19 recordsLinked to original sources
PubMed1990

Further thoughts on mast cells, calcium channels and histamine release.

Calcium movements across membranes of mast cells represent a major target for effective anti-allergic drugs, as these are essential events linking stimulation to secretion. Using isolated peritoneal mast cells from two types of genetically different rats and a blocker of the entry of calcium ions into cells, histamine release induced by antigen, calcium ionophore and potassium (in a lowered calcium medium) has been followed. Lower concentrations of the calcium entry blocker were required to inhibit potassium-induced release than those needed for release induced by allergic and other non-allergic stimuli, suggesting that different specialised calcium channels are involved in histamine release from rat mast cells.

Animals↗
PubMed1987

Calcium channels and histamine release from mast cells.

Using isolated peritoneal mast cells from two types of genetically different rats, histamine release induced by allergic stimuli was inhibited, in all cases except one, by significantly lower concentrations of an intracellular calcium antagonist than those required to inhibit release induced by a calcium ionophore. The exception related to inhibition of histamine release induced by clinical dextran in NR rats (which are relatively less sensitive to dextran than are control rats) as the concentrations required were of a similar order as those needed to inhibit release by ionophores. The data further support the suggestion that there are different calcium channels involved in the different release processes.

Animals↗
PubMed1986

Calcium and histamine release from mast cells.

The role of calcium in the process of histamine release from isolated rat peritoneal mast cells and in the pathophysiology of immediate hypersensitivity reactions has been further studied using the intracellular calcium antagonist, TMB-8. Inhibition by TMB-8 of histamine release from mast cells induced by allergic stimuli was found but higher concentrations were needed for reducing release induced by ionophores and activators of calcium gates. This suggests that there are different calcium channels involved in the different release processes.

Animals↗
PubMed1985

Thoughts on mast cells, histamine release and immunoglobulin E.

It is well known that the polysaccharide, dextran, stimulates rat mast cells to undergo histamine secretion, probably by interaction with cell-fixed IgE. Passive sensitisation with antigens greatly enhances histamine release induced in vitro by dextran, and removal of IgE from the cells by acid pH abolishes this release. The importance of IgE antibodies for histamine release from mast cells by agents other than dextran is also well recorded. For example, acetylcholine induces a non-immunological release which is potentiated by the presence of IgE. A link may also exist between cholinergic agents and substance P, a polypeptide which releases histamine by acting on specific receptors and not through interaction with cell-bound IgE. Attempts are made here to gather together some of the physiological and pathological processes involved.

Acetylcholine↗
PubMed1984

Histamine release from mast cells of the rat.

The relative activities of 12 agents inducing anaphylactoid oedema in the paws of two types of genetically different rats have been compared with those inducing histamine release from isolated peritoneal cells. Four groups were identified - group 1 where activities were much higher in R rats than in NR rats, doses in vivo being in all cases much lower than those required in vitro; group 2 where activities were similar in the two types of rat, doses in vivo again being relatively much lower; group 3 where activities were similar in both types of rat though doses in vivo were relatively high; group 4 where activities were similar in both types of rat, but doses in vivo were relatively extremely high. Only the activities of releasers in groups 1, 2 and 3 (represented by dextran, concanavalin A and antigen) required calcium ions in vitro and were potentiated by phosphatidyl serine; they were potentiated in vivo by insulin and inhibited by glucose.

Animals↗
PubMed1983

Histamine release by phosphatidic acid from isolated mast cells of two types of genetically different rats.

Phosphatidic acid produced a similar dose-dependent release of histamine from isolated peritoneal mast cells of two types of rat, one of which did not release histamine when dextran was present in the incubation mixture. This release induced by phosphatidic acid resembled that evoked by a basic secretagogue like compound 48/80, being independent of exogenous calcium and unaffected by either phosphatidyl serine or its lyso derivative. The non-cytotoxic release of histamine induced by phosphatidic acid is therefore distinct from that by dextran and does not involve dextran receptors residing on the plasma membrane of mast cells of rats which show the dextran anaphylactoid reaction.

Animals↗
PubMed1983

Proteins in the plasma membranes of rat peritoneal mast cells.

Plasma membranes of peritoneal mast cells from rats specifically bred for resistance to the dextran anaphylactoid reaction contain a polypeptide of molecular weight about 74,000 daltons which is deficient in those from rats which react to dextran. This polypeptide may modify the dextran receptor on the mast cell membranes of resistant rats so that histamine release does not take place when these cells are challenged with clinical dextran.

Animals↗
PubMed1983

Heparin and the dextran anaphylactoid reaction in rats.

Injections of heparin had no effect on the dextran anaphylactoid reaction in rats but neutralised the inhibitory action both of protamine and of borate. Heparin, protamine, and borate did not modify the histamine or 5-hydroxytryptamine responses in rat paws and so their effects on dextran may be due to modification of the release mechanisms of these two amines from tissue mast cells.

Anaphylaxis↗
PubMed1983

Enhancement of the anaphylactoid reaction in rats by phenylalanine enamine.

Low doses of phenylalanine enamine, administered at the same time as dextran, significantly enhanced the onset, height and duration of the anaphylactoid reaction in rats. The enhancement occurred after intraperitoneal or local administration. The enamine did not modify the histamine or 5-hydroxytryptamine responses in rat paws, so its effect on dextran may be due to modification of the release mechanism of the two amines from tissue mast cells.

Adjuvants, Immunologic↗
PubMed1983

Histamine releasers and rat mast cells.

The release of histamine from rat tissues rich in mast cells, induced by antigen, concanavalin A, dextran, compound 48/80, A 23187, phosphatidic acid and chlortetracycline, has been compared with that from isolated peritoneal mast cells of rats. Whereas most of the agents were more active than dextran in in vitro experiments, the reverse was found when they were injected intradermally into the skin, or subcutaneously into the paws. In fact, A 23187 and chlortetracycline (both calcium ionophores), as well as phosphatidic acid (another non-cytotoxic releaser), failed to release significant amounts of histamine when injected into the animal. Thus, the experimental conditions in which comparisons of the activities of histamine releasers are made should always be stated.

Animals↗