Factors influencing the urinary excretion of histamine in the rat

Wilson, C. W. M.

doi:10.1113/jphysiol.1954.sp005199

Cited by 18 publications

(3 citation statements)

References 15 publications

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“…The problem of a possible chemical counterregulation involving histamine release following sympathetic activity was further examined by WILSON [32] in the rat, by WENT and VARGA [33] in the dog, and SZILAGYI, K6V~R and CSABA [34] in the same animal species. WILSON [32] detected an increase of urinary excretion of histamine after intraperitoneal injection of large amounts of adrenaline.…”

Section: A Histamine Release By Adrenergic Drugs: In Vivo Experimentsmentioning

confidence: 99%

Modulation of the spontaneous histamine release by adrenergic and cholinergic drugs

et al. 1978

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Experiments have been reported on the possible modulation of the spontaneous histamine release by adrenergic and cholinergic drugs. Adrenergic drugs increase the spontaneous histamine release in vivo, and in neoplastic mast cells, in vitro. The mechanism of histamine release appears to be dependent upon the activation of alpha-adrenoceptors. Cholinergic drugs activate the release of histamine in many secretory processes in vivo; in vitro, acetylcholine is one of the most powerful histamine releasers in isolated purified rat mast cells. The release of histamine evoked by acetylcholine in rat mast cells is a calcium-requiring, temperature-dependent exocytosis. The physiological relationship of the sympathetic, parasympathetic and histamine-containing cells are discussed.

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Section: A Histamine Release By Adrenergic Drugs: In Vivo Experimentsmentioning

confidence: 99%

Modulation of the spontaneous histamine release by adrenergic and cholinergic drugs

et al. 1978

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“…Koch & Szerb (1950) had shown that adrenaline increases the amount of histamine liberated from lung of the rat perfused with Ringer solution. Wilson (1954) detected an increase of urinary excretion of histamine after intraperitoneal injection of a large amount of adrenaline in the rat. However, Mongar &!…”

Section: Introductionmentioning

confidence: 99%

The influences of adrenolytic drugs and noradrenaline on the histamine release in cardiac anaphylaxis in vitro

Giotti¹,

Guidotti²,

Mannaioni³

et al. 1966

The Journal of Physiology

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SUNMARY1. The regional distribution (auricles, ventricles and septum) of histamine and its release during anaphylaxis were studied in isolated perfused guinea-pig hearts.2. The highest value of histamine content was found in the right auricle, the lowest in the left ventricle and septum, both in normal hearts, and in the hearts subjected to anaphylaxis.3. The fraction of the total histamine released in the course of 24 mi by antigen was 50%. The fraction released from the different regions of the heart was similar. No evidence was found for release of 5-hydroxytryptamine. 4. A relation was found between the distribution of mast cells and the tissue concentration of histamine. The highest number of mast cells per unit area was found in the right auricle; the lowest in the left ventricle.5. The histamine release by antigen was reduced by previous treatment with (+)-tubocurarine; the histamine release by (+)-tubocurarine was depressed by previous challenge of the heart with antigen.6. Reserpine reduces histamine release. Perfusion of reserpine-treated hearts with noradrenaline partially restored histamine release.7. fl-Adrenergic blocking agents (dichloroisoproterenol and pronethalol) reduced histamine release.8. The drugs tested did not modify the tissue concentration of histamine.9. The possibility of a modulating activity of catecholamines on histamine release in cardiac anaphylaxis is discussed. ADRENOTROPIC DRUGS IN CARDIAC ANAPHYLAXIS 925 INTRODUCTIONWhile studying the occurrence of catecholamine release from a perfused heart in anaphylaxis, it was found that preliminary treatment with dichloroisoproterenol reduced the functional alterations as well as the release of histamine caused by the antigen (Mannaioni, Levi & Giotti, 1961 a, b). This finding led us to consider the hypothesis that catecholamines which leak from sympathetic nerve endings in the perfused heart (Hukovid & Muscholl, 1962) favour the anaphylactic release of histamine. It was indeed known that adrenaline injections increase the histamine level in the blood. This effect had been described by Anrep, Barsoum & Talaat (1936) on the heart-lung preparation of the dog and successively confirmed by Eichler & Barfuss (1940) in the intact cat and by Staub (1946) in humans. Koch & Szerb (1950) had shown that adrenaline increases the amount of histamine liberated from lung of the rat perfused with Ringer solution. Wilson (1954) detected an increase of urinary excretion of histamine after intraperitoneal injection of a large amount of adrenaline in the rat. However, Mongar &! Whelan (1953) did not obtain any change in plasma histamine concentration upon intravenous infusion of adrenaline either in man or in the cat.On the other hand, information on the effect of catecholamines on the anaphylactic release of histamine was scarce. Schild (1936) had described that a treatment with adrenaline decreased the release of histamine from perfused guinea-pig lungs submitted to anaphylaxis. The dose of adrenaline used in Schild's experiments did not allow ...

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“…Methylhistamine excretion was comparable in control and imidazole groups but was grea~ly reduced in guanethidine-treated rats. Wilson ( 1954) has shown that intraperitoneal injections of low doses of compound 48/80 (20-100 pg;kg) caused a twofold increase in histamine excretion; however, the hidamintiria rcturned to normal 90 min later. Schayer et al ( 1954), using a large dose of compound 48/80 ( 4 mg/kg) and 1 8.5-h urine collection, found that "no detectable portion of the histamine released by 48/80 reached the urine."…”

Section: Protocol and Resultsmentioning

confidence: 99%

Effects of Guanethidine and Imidazole on Histamine Metabolism

Doré¹,

LeBlanc²,

Côté³

1974

Can. J. Physiol. Pharmacol.

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D O R~, F., LEBLANC, J., and C 8~6 , J. 1974. Effects of guanethidine and imidazole on histamine metabolism. Can. J. Physiol. Pharmacol. 52,[978][979][980][981][982][983] Chronic treatment with guanethidine increased histamine excretion, as shown in a previous paper (Can. J. Physiol. Pharmacsl. 50, 539-544 (1972)). This increase was due to a partial inhibition of a degradation enzyme, imidazole N-methyltransferase, rather than to histamine liberation. Testosterone and noradrenaline diminished the high histaminuria caused by guanethidine. Irnid'azole, which was also shown to increase histamine excretion, was not affected by testosterone or noradrenaline. The mode s f action of inlidazole is still unknown, but its molecular configuration sriggests competitive effects with histamine at Inany sites.

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Factors influencing the urinary excretion of histamine in the rat

Cited by 18 publications

References 15 publications

Modulation of the spontaneous histamine release by adrenergic and cholinergic drugs

Modulation of the spontaneous histamine release by adrenergic and cholinergic drugs

The influences of adrenolytic drugs and noradrenaline on the histamine release in cardiac anaphylaxis in vitro

Effects of Guanethidine and Imidazole on Histamine Metabolism

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