Disease relevance of Hrh1

• We studied the effects of the histamine H1 receptor antagonists diphenhydramine and pyrilamine, the H2 receptor antagonist ranitidine and the muscarinic receptor antagonist atropine injected into the third cerebral ventricle on prostaglandin F2 alpha (PGF2 alpha)-induced hyperglycemia in anesthetized fed rats [1].
• The effect of perivagal capsaicin treatment on gastric acid secretion induced by the histamine H2 receptor agonist, dimaprit dihydrochloride, and the effect of the histamine H1 receptor agonist, 2-thiazolylethylamine dihydrochloride, on gastric acid secretion were studied in acute gastric fistula rats anesthetized with urethane [2].
• 2. Intraperitoneal pretreatment with cetirizine inhibited eosinophilia induced by either PAF (ED50 = 19 mg kg-1) or compound 48/80 (ED50 = 14 mg kg-1) whereas meclizine, another histamine H1-receptor antagonist, was inactive [3].
• Blocking the histamine H1 receptor might help to prevent or minimize leukocyte infiltration in uveitis [4].
• Rats treated with temelastine (SK&F 93,944), a novel histamine H1-receptor antagonist, develop thyroid lesions characterized by hypertrophy and colloid depletion [5].

Psychiatry related information on Hrh1

• These results suggest that feeding induced by histamine H1-receptor antagonists is due to blockade of neuronal histamine at the site of histamine H1-receptors, at least in part, in the ventromedial hypothalamus and that diurnal fluctuation of feeding behavior may reflect circadian variation of neuronal histamine level [6].

High impact information on Hrh1

• Lamellar bodies appear to be induced in the presence of histamine H1 receptor-blocking agents, since methaphenilene and diphenhydramine produced this reaction, but cimetidine, an H2 antagonist, did not [7].
• The decreased K(D) value in nonstimulated amygdala observed until 1 month after the last kindled seizure indicates the long-lasting increment of binding affinity of the pyrilamine binding site of the histamine H1 receptor in the steady state of kindled seizure susceptibility [8].
• The increase in paw volume produced by fluoxetine was inhibited by ketanserin (5-HT2 receptor antagonist), mepyramine (histamine H1 receptor antagonist) and phentolamine (alpha-adrenergic receptor antagonist), but not by the other selective 5-HT receptor antagonists tested or caffeine [9].
• Lesions of the neuronal histaminergic system or pharmacological blockade of histamine receptors, e.g., with histamine H1 receptor antagonists, can enhance the performance of rats in several tests of learning and memory [10].
• Histamine H1 receptor antagonists produce increases in extracellular acetylcholine in rat frontal cortex and hippocampus [10].

Chemical compound and disease context of Hrh1

• However, edema formation was significantly inhibited by treatment with pyrilamine, indicating that the histamine H1 receptor plays a critical role in PPV-induced formation of acute edema [11].
• In the present study the effect of mizolastine (CAS 108612-45-9, SL85.0324-00) a novel potent histamine H1-receptor antagonist, on 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis, a rat model of inflammatory bowel disease, was investigated to determine whether mizolastine has anti-inflammatory properties [12].

Biological context of Hrh1

• A rat histamine H1 receptor gene which lacked introns was isolated from a rat genomic library using recently cloned bovine histamine H1 receptor cDNA [Yamashita et al., Proc. Natl. Acad. Sci. USA, 88, 11515-11519 (1991)] [13].
• The histamine H1 receptor antagonist mepyramine (0.4 or 0.8 microg) had no significant effect on population spikes or field excitatory postsynaptic potentials [14].
• Pretreatment with a dose of more than 20 mg/kg of histamine H1-receptor antagonists such as tripelennamine or diphenhydramine prior to the injection of compound 48/80 (3.0 mg/kg s.c.) attenuated or abolished the effects of compound 48/80 on PRA, hematocrit and plasma extravasation [15].
• Administration of histamine (40-80 microg/rat) and naloxone (0.5-1 microg/rat) increased, while morphine (2.5 microg/rat), pyrilamine (25-50 microg/rat), the histamine H1 receptor antagonist, and ranitidine (10-20 microg/rat), the histamine H2 receptor antagonist, decreased water intake in isolated rats [16].
• Electrophoretic application of a histamine H1-receptor antagonist to ventromedial hypothalamic neurons specifically suppressed activities of glucose-responding neurons that are related to food intake [6].

Anatomical context of Hrh1

• Northern blot analysis detected a 3.0 kb nucleotide band for histamine H1 receptor mRNAs from rat brain and small intestine when these mRNAs were hybridized with the isolated rat H1 gene [13].
• Activation of histamine H1-receptor enhances neurotrophic factor secretion from cultured astrocytes [17].
• However, prior treatment with mepyramine (a histamine H1 receptor antagonist) neither attenuated the changes in water content and the blood-brain barrier permeability nor altered the cerebral blood flow and 5-hydroxytryptamine levels [18].
• These results suggest that alpha-mangostin is a novel competitive histamine H1 receptor antagonist in smooth muscle cells [19].
• The histamine H1 receptor agonist, 2-pyridyl-ethylamine, produced a relaxant response only in progesterone dominant uterus [20].

Associations of Hrh1 with chemical compounds

• The specific histamine H3 receptor antagonist, clobenpropit (3.0 mg kg(-1), i.v.), blocked the inhibitory effect of R-alpha-methylhistamine, whereas neither the histamine H2 receptor antagonist, cimetidine (5.0 mg kg(-1), i.v.), nor the histamine H1 receptor antagonist, chlorpheniramine (0.5 mg kg(-1), i.v.), was effective [21].
• The ED50 was increased 10-fold by 0.1 microM chlorpheniramine (a histamine H1-receptor selective antagonist) [22].
• 7. The selective histamine H1-receptor agonist, 2-pyridyl ethylamine, had no effect on acid output but increased resting mucosal blood flow [23].
• Thioperamide also induced an increase in SS binding in rats pretreated with mepyramine, a histamine H1-receptor antagonist, or cimetidine, a histamine H2-receptor antagonist [24].
• The effect was inhibited by hexamethonium, lignocaine, or by the tachykinin antagonist (D-Pro2, D-Trp7,9)-SP, but not by atropine, or by a combination of the histamine H1-receptor antagonist chlorpheniramine and the H2-receptor antagonist ranitidine [25].

Regulatory relationships of Hrh1

• Cell proliferation in dimethylhydrazine-induced colonic carcinomata was stimulated by histamine and by the histamine H2 receptor agonist dimaprit and inhibited by the histamine H2 receptor antagonists Metiamide and Cimetidine but not by the histamine H1 receptor antagonist Mepyramine [26].

Other interactions of Hrh1

• Preincubation of the preparation with indomethacin (10(-6) M), the histamine H1 receptor antagonist, pyrilamine (10(-8) M), and the histamine H3 receptor antagonist, clobenpropit (10(-8) M), decreased the oral contraction by 60.1+/-7.7%, 42.8+/-6.9% and 44.4+/-14.2% as well as the anal relaxation [27].
• This oestrogen-induced increase of blood flow was reduced significantly by pretreatment with mepyramine (a histamine H1-receptor antagonist), cellulose sulphate (a kininogen-depleting agent) and aprotinin (a kininogenase inhibitor) [28].
• The effect of compound 48/80 on plasma insulin-like growth factor I was significantly attenuated by oral administration of the histamine H1 receptor antagonist (chlorpheniramine), but not by the histamine H2 receptor antagonists (cimetidine and ranitidine) [29].
• GBR 12909 was a potent and selective inhibitor of synaptosomal dopamine uptake (KI = 1 nM), with a 20-fold lower affinity for the histamine H1-receptor and a more than 100-fold affinity for the noradrenaline and 5-HT uptake carriers, the dopamine D-1, D-2, 5-HT2, 5-HT1A and alpha 1-receptors and voltage-dependent sodium channels [30].
• GABAB receptor-mediated inhibition of histamine H1-receptor-induced inositol phosphate formation in slices of rat cerebral cortex [31].

Analytical, diagnostic and therapeutic context of Hrh1

• Guinea pig histamine H1 receptor. I. Gene cloning, characterization, and tissue expression revealed by in situ hybridization [32].
• However, the presence of histamine H1 receptor antagonists in the perfusion medium abolished (+/-)-MDMA-induced ACh release [33].
• Moreover, stimulation with SGFO elevated the plasma glycerol level, and treatment with either ZnSO4 or an intraperitoneal injection of diphenhydramine, a histamine H1 receptor-antagonist, abolished the glycerol elevation by SGFO [34].
• A high-performance liquid chromatographic (HPLC) method for the quantitative determination of epinastine, a non-sedating histamine H1 receptor antagonist, in rat plasma, was developed [35].
• Southern blot analysis showed that there was another gene quite similar to the cloned histamine H1 receptor gene [36].

References