Histamine-Releasing Effect of a Corticotrophin Derivative

1. The basic peptide substance P causes histamine release from peritoneal mast cells of the rat in vitro whereas the closely related neutral peptides eledoisin and physalaemin do not. 2. Infusion of substance P (7.4 nmol min-1), but not of eledoisin (8.4 nmol min-1) or physalaemin (7.9 nmol min-1), into the rat hindquarter preparation caused a more than 4-fold increase of the histamine content in the venous outflow. The outflow of 5-HT remained unchanged under infusion of all three peptides. 3. No histamine depletion in the skin of the rat hind paw was observed following antidromic stimulation of the saphenous nerve or cutaneous application of mustard oil. Infusion of substance P (7.4 nmol min-1) caused a 47% depletion of histamine in the paw skin although only a small proportion of the infused substance P seemed to enter the tissue from the blood vessels. 4. The results further substantiate the view that substance P upon release from peripheral nerve endings induces release of histamine from cutaneous mast cells, a mechanism which contributes to neurogenic vasodilatation and plasma extravasation.

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Release of histamine by substance P

Erjavec

Lembeck

Florjanc-Irman

et al. 1981

Naunyn-Schmiedeberg's Arch. Pharmacol.

166

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Dysrhythmias caused by histamine release in guinea pig and human hearts

et al. 1982

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Histamine is released into the systemic circulation during anaphylaxis, by drugs and by surgical procedures. Studies in animal models have conclusively demonstrated that released cardiac histamine is a major mediator of arrhythmias that occur during anaphylaxis and following the administration of histamine-releasing drugs. Several lines of evidence suggest a similar arrhythmogenic role for cardiac histamine in humans: (1) The human heart is rich in histamine; (2) cardiac histamine can be readily released from human heart in vitro by therapeutic concentrations of drugs; (3) histamine has potent arrhythmogenic effects on the human heart in vitro. Arrhythmogenic effects of histamine include enhancement of normal automaticity, induction of abnormal automaticity, induction of triggered tachyarrhythmias, depression of atrioventricular conduction, and increase in the vulnerability of the ventricles to fibrillation. A combination of H1 and H2 antihistamines is needed to block the arrhythmogenic effects of histamine. Certain arrhythmogenic effects of histamine (e.g. induction of slow responses and delayed afterdepolarizations) can also be blocked by drugs which inhibit the influx of cations through slow channels. In contrast, the commonly-used drug digitalis potentiates the arrhythmogenic effects of histamine. We propose that histamine release produced by drugs and surgical procedures may be an overlooked factor in fatal cardiac arrhythmias. Experimental studies suggest that selective pharmacological methods can be developed to block the arrhythmogenic effects of histamine.

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The interaction of cholinomimetics, peptides and compounds 48/80 on histamine secretion from the mast cell

Erjavec

Iskra

1984

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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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Histamine-Releasing Effect of a Corticotrophin Derivative

Cited by 7 publications

References 12 publications

Release of histamine by substance P

Release of histamine by substance P

Dysrhythmias caused by histamine release in guinea pig and human hearts

The interaction of cholinomimetics, peptides and compounds 48/80 on histamine secretion from the mast cell

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