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Regulation Of Cell Kinetics And Colon Cancer
Published in Herman Autrup, Gary M. Williams, Experimental Colon Carcinogenesis, 2019
Two hormones within this group, histamine and serotonin, have been shown to stimulate cell division in colonic tumors, while another amine, epinephrine, inhibits tumor cell division. Note that neither metaraminol nor alpha-adrenergic antagonists influence tumor cell proliferation. Histamine, acting apparently via a histamine H2 receptor, has been shown to stimulate cell proliferation in DMH-induced rat colonic tumors but not in rat colonic crypt cells.59 The histamine H2-receptor agonist, dimiprit, had a similar effect. The histamine H2 receptor antagonists, cimetidine, metiamide, and ranitidine, slow down cell proliferation in rat colonic tumors and retard the growth of some human colonic tumors growing in immune-deprived mice.66,67
Neurohormonal Regulation of Gastric Mucosal Growth
Published in Jean Morisset, Travis E. Solomon, Growth of the Gastrointestinal Tract: Gastrointestinal Hormones and Growth Factors, 2017
Prolonged administration of metiamide61 and also of antacids62 has been found to induce hyperplasia of parietal cells in rats. No mitogenic effect could be observed when cimetidine was given to rats.63 Unfortunately, the interpretation of data on progenitor cell activity in human ulcer patients under cimetidine is unreliable because kinetic parameters measured after inadequate fasting periods are not reliable.64
Histamine as Neurotransmitter
Published in Divya Vohora, The Third Histamine Receptor, 2008
Oliver Selbach, Helmut L. Haas
Ionophoretic local application of histamine demonstrated functional histaminergic projections to the cortex [268]. Depressant actions of histamine were blocked by the H2R antagonist metiamide [12,311,312]. Intracellular recordings from human cortex revealed H2R-mediated excitatory actions through block of gK+(Ca2+) [181,241], as described in the hippocampus of several species including man [16]. Furthermore, H1R-mediated excitation of principal cortical neurons has been identified as the target of the sedative antihistaminics [188]. A perforated patch-clamp study in olfactory bulb slices from newborn rabbits has revealed outward and inward currents in inter-neurons through H1R and H2R, respectively, whereas no changes were observed in the principal mitral cells [187]. Both these currents reversed at the potassium equilibrium. GABAergic interneurons in the olfactory bulb represent a cell population that is continuously replaced by adult stem cells throughout life [313].
Activation of carbonic anhydrase isoforms involved in modulation of emotional memory and cognitive disorders with histamine agonists, antagonists and derivatives
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Gustavo Provensi, Alessio Nocentini, Maria Beatrice Passani, Patrizio Blandina, Claudiu T. Supuran
Some of these compounds, possessing structures 2–30 (Figure 1), were included in our study for investigating their possible CA activating effects against four pharmacologically relevant human isoforms, hCA I, II, IV and VII. The compounds were numbered according to their similarity to the lead histamine 1 and are: the H1R agonist 2-(2-aminoethyl)thiazole 6; the H2R agonists impromidine 16 and nordimaprit 19; the H3R agonists Nπ-methylhistamine 3, α-methylhistamine 4, methimmepip 8, proxyfan 9, imetit 14, VUF16839 23; the H1R antagonists pyrilamine 24, loratadine 29; the H2R antagonists metiamide 12, cimetidine 13, ranitidine 17, tiotidine 18, zolantidine 20; the H3R antagonists ciproxifan 10, clobenpropit 15, ABT239 22, GSK189254A 28, GSK334429B 30; the H4R antagonists JNJ39758979 25, JNJ7777120 26, A940894 27; the mixed modulators of the histaminergic system Nτ-methylhistamine 2, 4-methylhistamine 5, 1-methylhistidine 7, burimamide 11, betahistine 21.