The Mechanism of Histamine Release in Anaphylactic Reaction in Guinea Pig and Rat

Chakravarty, Nirmal

doi:10.1111/j.1748-1716.1960.tb01854.x

Cited by 96 publications

(41 citation statements)

References 25 publications

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“…Vascular tissue was first shown to release SRS-A more than 20 years ago (Brocklehurst, 1960;Chakravarty, 1960), and more recently it has been demonstrated that large peripheral blood vessels obtained from a variety of species, including the dog, possess the capacity to synthesize and release leukotriene-like substances Wolbling et al, 1983;Dembinska-Kiec et al, 1984). Although the formation of leukotrienes in vascular smooth muscle has not been unequivocally demonstrated, these derivatives stimulate vascular smooth muscle and may participate in vasomotor control mechanisms.…”

mentioning

confidence: 99%

Leukotriene D4 relaxes canine renal and superior mesenteric arteries.

Secrest¹,

Olsen²,

Chapnick³

1985

Circulation Research

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SUMMARY. To characterize the influences of leukotriene D 4 on regional vascular smooth muscle, effects of leukotriene D 4 on vasomotor tone of canine renal and superior mesenteric arterial rings were determined. Vascular smooth muscle tone was measured with isometric force transducers. After tone had been induced with norepinephrine, leukotriene D«, in concentrations of 10~* M to 10~7 M, produced dose-dependent relaxation of renal and superior mesenteric arterial rings. Leukotriene D 4 -induced relaxation was observed only in those ring preparations in which care had been taken to avoid damaging the Iuminal surface. Acetylcholine (10~7 M) also decreased tone in these same ring segments. Neither acetylcholine nor leukotriene D 4 altered tone of arterial rings after the endothelium had been intentionally disrupted by rubbing with a cotton-tipped applicator. Nitroglycerin (1CT* M) relaxed rings both before and after rubbing the intimal surface. These results demonstrate that leukotriene D 4 possesses the capacity to relax canine superior mesenteric and renal arterial rings in an endothelial-dependent manner. Because relaxation of renal and superior mesenteric arterial rings in response to leukotriene D 4 was not altered after incubation with indomethacin (10~! M), the observed endothelial-dependent relaxation induced by leukotriene D 4 did not appear to be related to release of a cyclooxygenase metabolites). In contrast, FPL 55712 (10~5 M) attenuated the relaxation produced by leukotriene D 4 , suggesting that this response was a receptor-linked consequence. (Circ Res 57: 323-329, 1985)

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mentioning

confidence: 99%

Leukotriene D4 relaxes canine renal and superior mesenteric arteries.

Secrest¹,

Olsen²,

Chapnick³

1985

Circulation Research

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“…Histamine release from guinea-pig lung induced by the antigen-antibody reaction is dependent on calcium (Mongar & Schild, 1958;Chakravarty, 1960) and the anaphylactic histamine release from rat mast cells is maximal at a calcium concentration of 1 to 2 x 10-' mol/l (Foreman & Mongar, 1972).…”

Section: Discussionmentioning

confidence: 99%

“…Anaphylactic histamine release from guinea-pig lung and disruption of rat mast cell due to antigen is dependent on the incubation temperature (Mongar & Schild, 1957;Chakravarty, 1960;Hogberg & Uvniis, 1960). Histamine release from guinea-pig lung induced by the antigen-antibody reaction is dependent on calcium (Mongar & Schild, 1958;Chakravarty, 1960) and the anaphylactic histamine release from rat mast cells is maximal at a calcium concentration of 1 to 2 x 10-' mol/l (Foreman & Mongar, 1972).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Histamine Release From Rat Mast Cells Induced by the Ionophore A23187: Effects of Calcium and Temperature

Johansen¹

1978

British J Pharmacology

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The mechanism of histamine release from a pure population of rat mast cells induced by the lipid soluble antibiotic, A23187, has been studied and compared with data for anaphylactic histamine release reported in the literature. Histamine release induced by A23187 in the presence of calcium 10−3 mol/1 was completed in 10 minutes. By preincubation of the mast cells with A23187 for lOmin in the absence of calcium the histamine release induced by calcium, 10−3 mol/1 or 5 × 10−3 mol/1, was completed in 90s and 45 s, respectively. A23187‐induced histamine release was maximal with calcium 10−3 mol/1 when the cells were incubated at 33 to 39°C for 10 minutes. The cellular mechanism, which was stimulated by A23187 and calcium for the release of histamine, was irreversibly inactivated by incubation at 45°C. An inhibition of energy metabolism was excluded as the cause of the heat inactivation. The dependence of A23187‐induced histamine release on calcium and temperature, the time course of histamine release and the heat inactivation are consistent with the view that the same mechanism is involved in A23187‐induced and anaphylactic histamine release.

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“…The anaphylactic histamine release from most organs of guinea pigs ranges between 25 and 33% of total organ histamine when tested in vitro without aminoguanidine protection [5,6]. The liver holds a unique posi- For calculation of recovery, the Ipasma histamine levels determined after the histamine injection were subtracted by 0.05 /(g/ml, i.e., the mean histamine level determined in the liver blood plasma of 3 animals not injected with histamine (0.05 ±0.01 //g/ml).…”

Section: Discussionmentioning

confidence: 99%

Liver Histamine and Zinc in Guinea Pig Anaphylaxis

Hahn¹,

Jobke²

1974

Int Arch Allergy Immunol

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The anaphylactic histamine release from guinea pig liver under amino-guanidine protection was studied in vivo by injecting antigen into the portal vein. No significant decrease of liver histamine could be observed 2 min after antigen, whereas a significant, though small increase of plasma histamine in the liver blood occurred indicating a histamine release of 1.2% of total liver histamine. When histamine was injected into the portal vein of normal guinea pigs at a dosage about 1.75 times the amount of total liver histamine, 48.8% or even more was retained by the liver. Since, on the basis of our previous studies on heparin release, the liver mast cell disintegration must be considered greater than is suggested by the extent of histamine output, much of the histamine released from the mast cells is probably taken up by the liver cells and metabolized. Zinc which is assumed to link histamine to heparin, was not increased in the liver blood plasma upon challenge with antigen. The guinea pig liver possibly acts as a buffer organ preventing histamine overload of the blood during anaphylaxis. It serves this function by binding hepatic as well as extrahepatic histamine, and in addition, by the heparin-mediated release and activation of liver histaminase which acts both locally and systemically.

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The Mechanism of Histamine Release in Anaphylactic Reaction in Guinea Pig and Rat

Cited by 96 publications

References 25 publications

Leukotriene D4 relaxes canine renal and superior mesenteric arteries.

Leukotriene D4 relaxes canine renal and superior mesenteric arteries.

Mechanism of Histamine Release From Rat Mast Cells Induced by the Ionophore A23187: Effects of Calcium and Temperature

Liver Histamine and Zinc in Guinea Pig Anaphylaxis

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