Histamine acid phosphate

Theory The gravimetric assay of histamine acid phosphate is based upon the formation of insoluble histamine-nitranilic acid complex as depicted in the following equation ... 

Dose. Histamine acid phosphate is given subcutaneously, in a dose of 40 ig/kg, following administration of a large dose of an antihistamine. 

Histamine Acid Phosphate Phenyltoloxamine Citrate Ketoconazole... 

Histamine acid phosphate, 659 Histamine dihydrochloride, 659 Histamine diphosphate, 659 Histamine hydrochloride, 659 Histamine phosphate, 659 Histantil, 932 Histapyrrodine, 660 Histapyrrodine hydrochloride, 660 Histaspan, 457 Histergan, 557 Histex, 433 Histryl, 560 Histylamine, 1022 HMMA, 322 HoggarN, 576... 

SYNS 4-(2-AMINOETHYL)MD.AZOLE BISpi-HYDROGEN PHOSPHATE) 4-(2-AMINOETHYL)-IMIDAZOLE DI-ACID PHOSPHATE HISTAMINE ACID PHOSPHATE HISTAXONE PHOSPHATE (1 2) 1H-IMIDAZOLE-4-ETHANAMINE PHOSPHATE (1 2)... 

In a single-dose evaluation, 6 jig./kg. of ICI 50,123 was equivalent to (XS /l S of histamine acid phosphate.° Ho synthetic derivatives of gastrin, other than those already reviewed,9 have been described. 

Histamine Acid Phosphate, B.P. C5H9N3,2H3P04 307-1 Nitranilic acid 0-9001... 

Among the compounds commonly determined in research laboratories are diacetyl, 2,3-butandiol, glycerol, citramalic acid, amino acids (especially proline), histamine, ammonia, succinic acid, phosphate, ash, alkalinity of the ash, ethyl, acetate, methyl anthranilate, total volatile esters, higher alcohols (both total and individually) phenolic compounds, etc. An elegant method for determining ethyl esters, capronate, caprylate, caprinate, and laurate using carbon disulfide extraction and GLC has been published (123). 

Note The pre- and post-treatment of the chromatograms with the basic tri-ethylamine solution, which can be replaced by an alcoholic solution of sodium hydroxide [1,4] or a phosphate buffer solution pH = 8.0 (c = 0.2 mol/1) [5], serves to stabilize the fluorescence of the amino derivatives [2]. A final spraying with methanolic hydrochloric acid (chci = 5 mol/1) or 70% perchloric acid renders the detection reaction highly specific for histamine [4] and for catecholamines and indolamines [5]. 

Histamine is synthesised by decarboxylation of histidine, its amino-acid precursor, by the specific enzyme histidine decarboxylase, which like glutaminic acid decarboxylase requires pyridoxal phosphate as co-factor. Histidine is a poor substrate for the L-amino-acid decarboxylase responsible for DA and NA synthesis. The synthesis of histamine in the brain can be increased by the administration of histidine, so its decarboxylase is presumably not saturated normally, but it can be inhibited by a fluoromethylhistidine. No high-affinity neuronal uptake has been demonstrated for histamine although after initial metabolism by histamine A-methyl transferase to 3-methylhistamine, it is deaminated by intraneuronal MAOb to 3-methylimidazole acetic acid (Fig. 13.4). A Ca +-dependent KCl-induced release of histamine has been demonstrated by microdialysis in the rat hypothalamus (Russell et al. 1990) but its overflow in some areas, such as the striatum, is neither increased by KCl nor reduced by tetradotoxin and probably comes from mast cells. 

Most people have heard of antihistamines, even if they have little concept of the nature of histamine. Histamine is the decarboxylation product from histidine, and is formed from the amino acid by the action of the enzyme histidine decarboxylase. The mechanism of this pyridoxal phosphate-dependent reaction will be studied in more detail later (see Section 15.7). 

The principal pathways for the biogenesis and metabolism of histamine are well known. Histamine is formed by decarboxylation of the amino acid, L-histidine, a reaction catalyzed by the enzyme, histidine decarboxylase. This decarboxylase is found in both mammalian and non-mammalian species. The mammalian enzyme requires pyridoxal phosphate as a cofactor. The bacterial enzyme has a different pH optimum and utilizes pyruvate as a cofactor (26.27). 

Decarboxylation, or loss of the a-carboxyl group as C02, is another reaction common to most amino acids. It, too, requires pyridoxal phosphate as a coenzyme. Decarboxylation reactions are irreversible. For example, see Figure 20.5, which shows the decarboxylation of histidine to produce histamine. Table 20.6 lists transamination and decarboxylation products of some representative amino acids. 

Histamine, serotonin and the catecholamines (dopamine, epinephrine and norepinephrine) are synthesized from the aromatic amino acids histidine, tryptophan and phenylalanine, respectively. The biosynthesis of catecholamines in adrenal medulla cells and catecholamine-secreting neurons can be simply summarized as follows [the enzyme catalysing the reaction and the key additional reagents are in square brackets] phenylalanine — tyrosine [via liver phenylalanine hydroxylase + tetrahydrobiopterin] —> i.-dopa (l.-dihydroxyphenylalanine) [via tyrosine hydroxylase + tetrahydrobiopterin] —> dopamine (dihydroxyphenylethylamine) [via dopa decarboxylase + pyridoxal phosphate] — norepinephrine (2-hydroxydopamine) [via dopamine [J-hydroxylasc + ascorbate] —> epinephrine (jV-methyl norepinephrine) [via phenylethanolamine jV-methyltransferase + S-adenosylmethionine]. 

Exchange of the nicotinamide moiety of NADP for nicotinic acid, forming NAADP. Early studies also showed that the enzyme can catalyze exchange of nicotinamide with a variety of other bases, including histamine. Formation of histamine adenine dinucleotide phosphate was thought to provide an alternative to amine oxidase for rapid inactivation of histamine. 

Dog A, female, 13 kg, gastric fistula and esophagotomy, operated March 1945. Sections A and B represent an experiment of November 22, 1948, and section C an experiment of January 4, 1949. In the latter 2 mg atropine sulfate were injected 42 minutes before the injection of histamine phosphate. Rate of secretion and concentration of total acid and pepsin are shown by line graphs in order to more completely characterize the samples. The spontaneous mucus specimens represent 30-minute samples. UA = uronic acid HN = total hexosamine HN = excess hexosamine mmoles/liter. From Grossberg et al. (G70). 

The enzymes, amino acid decarboxylases are pyridoxal phosphate- dependent enzymes. Pyridoxal phosphate forms a Schiff s base with e amino acid so as to stabilise the a-carbanion formed by the cleavage of bond between carboxyl and a-carbon atom. The physiologically active amines epinephrine, nor-epinephrine, dopamine, serotonin, y-amino butyrate and histamine are formed through decarboxylation of the corresponding precursor amino acids... 

Histamine, an amine produced in numerous tissues throughout the body, has complex physiological effects. It is a mediator of allergic and inflammatory reactions, a stimulator of gastric acid production, and a neurotransmitter in several areas of the brain. Histamine is formed by the decarboxylation of L-hisddine in a reaction catalyzed by histidine decarboxylase, a pyridoxal phosphate-requiring enzyme. 

Figure 2.13. Histamine H,-receptor-mediated inositol phospholipid hydrolysis. Stimulation of H,-receptors leads to activation of a phospholipase C. probably via a guanine-nucleotide regulatory protein (N). which catalyses the hydrolysis of phosphatidylinositol 4.5 -bisphosphate (PIP2) to give inositol trisphosphate (IP3) and 1,2-diacylglycerol (DG). IP3 is then broken down by phosphatases to eventually yield free myo-inositol. Lithium ions can inhibit the conversion of inositol 1-phosphate (IP,) to myo-inositol. Free inositol then interacts with CDP-diacylglycerol,formed by a reaction between phosphatidic acid (PA) and CTP, to yield phosphatidylinositol (PI). Phosphorylation of PI by kinases completes the lipid cycle by reforming PIP2. Modified from [147,148].

I, 4-bisphosphate and inositol 1,4,5-trisphosphate [59,60]. More recent studies, however, have shown that acid conditions are necessary for the extraction of these latter inositol phosphates [238]. With this modification to the experimental protocol it is possible to demonstrate a rapid accumulation of inositol trisphosphate in slices of guinea-pig cerebellum in response to histamine [238]. The rate of accumulation of inositol trisphosphate in this brain region is more rapid than that of the less polar inositol phosphates and the highest rate of accumulation is normally achieved during the first 5 min of... 

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