Metabolism and Excretion of Histamine

Schayer, Richard W.; Wetterqvist, H.; Beaven, M A; Horakova, Zdenka

doi:10.1007/978-3-642-66445-8_3

Cited by 9 publications

(11 citation statements)

References 268 publications

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“…Histamine in tissues is believed to derive mostly from decarboxylation of histidine, (see Schayer, 1978), yet injections of histidine do not increase histamine levels in all tissues of mouse and rat containing decarboxylases (Taylor and Snyder, 1972;Schwartz etal., 1972;Huszti et al, 1977;Endo, 1979). This is a surprising finding, for histidine can be decarboxylated by both histidine decarboxylase, i.e., E.C.…”

Section: Metabolism Of Histaminementioning

confidence: 97%

“…A full and fair review of histamine metabolism would be voluminous, hence the discussion here is confined to some recent work and to work that shows questions that need to be answered. Reviews have appeared on the metabolism of histamine (e.g., Schayer, 1978;Wetterqvist, 1978;Beaven, 1982;Code, 1985). As shown in Fig.…”

Section: Metabolism Of Histaminementioning

confidence: 97%

“…3 shows two methylhistamines that could, in principle, be formed by metabolism: tele-methylhistamine, also named Nr-methylhistamine (i.e., t-MH) and pros-methylhistamine or N~-methylhistamine (i.e., p-MH). t-MH is by far the dominant methylated metabolite formed (see Schayer, 1978;Wetterqvist, 1978;Beaven, 1982;Code, 1985). Endogenous t-MH has been found in human body fluids (see Keyzer etal., 1981;Swahn and Sedvall, 1981;Kahndelwal etal., 1982a;Imamura etal., 1984b) and in tissues (Green, 1970;Hough etal., 1979Hough etal., , 1981Oishi et al, 1984;Imamura et al, 1984b).…”

Section: Metabolism Of Histaminementioning

confidence: 97%

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Aspects of histamine metabolism

et al. 1987

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Section: Metabolism Of Histaminementioning

confidence: 97%

Section: Metabolism Of Histaminementioning

confidence: 97%

Section: Metabolism Of Histaminementioning

confidence: 97%

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Aspects of histamine metabolism

et al. 1987

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“…Histidine decarboxylase (HDC), the key enzyme/rate‐limiting enzyme in the synthesis of histamine, is an adaptive enzyme that is induced by various stimuli . Prolonged physical exercise or walking induces HDC in the skeletal muscles of mice .…”

Section: Introductionmentioning

confidence: 99%

Roles played by histamine in strenuous or prolonged masseter muscle activity in mice

Yoneda

Yaoita

Tsuchiya

et al. 2013

Clin Exp Pharma Physio

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Bruxism and/or clenching, resulting in fatigue or dysfunction of masseter muscles (MM), may cause temporomandibular disorders. Functional support of the microcirculation is critical for prolonged muscle activity. Histamine is a regulator of the microcirculation and is supplied by release from its stores and/or by de novo production via the induction of histidine decarboxylase (HDC). Interleukin (IL)-1, a cytokine involved in temporomandibular disorders, is an inducer of HDC. In the present study, we examined the roles of histamine, HDC and IL-1 in MM activity. Experiments were conducted using our R+G+ model. A mouse restrained (R+) inside a narrow cylinder (front end blocked with a thin plastic strip) gnaws away (G+) the strip to escape, with the weight reduction in the strip serving as an index of MM activity. Fexofenadine (a peripherally acting histamine H1 receptor antagonist) reduced MM activity in normal mice. Both H1 receptor-deficient and HDC-deficient mice exhibited low MM activity. Prolonged R+G+ induced HDC activity in MM. Mast cell-deficient mice exhibited strikingly low HDC induction in MM (and also in the quadriceps femoris muscle) in response to muscle activity or IL-1β. Mast cells were present around blood vessels and nerves in the epimysium and perimysium of MM. These results, together with others reported previously, suggest that: (i) peripheral histamine supports strenuous MM activity; (ii) strenuous MM activity stimulates mast cells to release histamine and to induce HDC (which replenishes the histamine pool in mast cells, possibly mediated by IL-1); and (iii) peripheral histamine H1 receptor antagonists may be effective in treating temporomandibular disorders or preventing prolonged clenching and/or bruxism.

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“…It is also known that the histamine-forming enzyme, histidine decarboxylase (HDC), is a typical adaptive enzyme induced in response to a variety of stimuli. [6][7][8][9][10] The histamine newly formed via HDC induction is released without being stored, [7][8][9][10][11] and it has been suggested that histamine from this source is involved both in the regulation of the microcirculation 8,9) and in anabolic processes during rapid cell growth. 7) Interestingly, prolonged walking (PW) (or other prolonged physical exercise) induces HDC in mouse skeletal muscles, [12][13][14][15] and the elevation of HDC activity persists for several hours after the exercise ends.…”

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confidence: 99%

Roles of Histamine in Exercise-Induced Fatigue: Favouring Endurance and Protecting against Exhaustion

Yaoita

Tsuchiya

Ohtsu

et al. 2012

Biological & Pharmaceutical Bulletin

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Exercise necessitates a large supply of O 2 and nutrients and rapid removal of CO 2 and waste products. Histamine is a regulator of the microcirculation (which performs these exchanges), suggesting a possible involvement of histamine in exercise. Histamine is released from either mast cells or non-mast cells. In the latter, histamine is newly formed via the induction of histidine decarboxylase (HDC) in response to an appropriate stimulus, and it is released without being stored. Here, in mice, we examined the role of histamine or HDC induction in exercise. Prolonged walking (PW) (in a cylindrical cage turned electrically) increased HDC mRNA and HDC activity in quadriceps femoris muscles. Mice given a histamine H1-receptor antagonist [fexofenadine (peripherally acting) or pyrilamine (peripherally and centrally acting)] or an irreversible HDC inhibitor (α-fluoromethylhistidine) displayed less PW endurance than control mice. Ranitidine (H2-receptor antagonist) tended to reduce endurance. Other histamine-receptor (H3 and H4) antagonists had no significant effects on endurance. Mice deficient in HDC or histamine H1-receptors displayed markedly less endurance than control mice, and HDC activity in the quadriceps femoris of H1-deficient mice was rapidly elevated by PW. Fexofenadine significantly reduced the muscle levels of nitric oxide (NO) metabolites and glycogen after PW. The results support the ideas that (i) histamine is involved in protecting against exerciseinduced fatigue or exhaustion, (ii) histamine exerts its protective effect via H1 receptors and the ensuing production of NO in skeletal muscle, and (iii) histamine is provided, at least in part, by HDC induction in skeletal muscles during prolonged exercise.

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Metabolism and Excretion of Histamine

Cited by 9 publications

References 268 publications

Aspects of histamine metabolism

Aspects of histamine metabolism

Roles played by histamine in strenuous or prolonged masseter muscle activity in mice

Roles of Histamine in Exercise-Induced Fatigue: Favouring Endurance and Protecting against Exhaustion

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