Disease relevance of Pyranisamine

• Ethanol-induced hyperemia was markedly reduced by lipoxygenase-selective inhibitors BW755C or nordihydroguaiaretic acid, or by the H1-antihistamine pyrilamine, but not by indomethacin, cimetidine, phentolamine, or methysergide [1].
• These hosts were protected from systemic anaphylaxis by treatment with the anti-histamine mepyramine [2].
• However, in combination with pyrilamine, the hypotension was substantially reduced [3].
• In the current study, actively sensitized guinea pigs treated three times daily with H-1 (mepyramine) and H-2 (cimetidine) histamine receptor antagonists, during the challenge tick infestation period, expressed normal resistance to Amblyomma americanum larvae [2].
• Release of histamine occurred at tick feeding sites, but vasoactive effects were blocked by mepyramine treatment as evidenced by a lack of increased vascular permeability (bluing) at these sites compared with non-tick-infested tissues, or to cutaneous basophil hypersensitivity (CBH) sites of animals not protected with mepyramine [2].

Psychiatry related information on Pyranisamine

• The effects of HA were attenuated by systemic or in situ pretreatment with mepyramine (an H1-receptor antagonist), which when injected alone produced an increase in slow wave sleep [4].
• Similarly, injections of mepyramine (120 micrograms/1 microliter) in the same structures caused a significant decrease in wakefulness and an increase in deep slow wave and paradoxical sleep as well [5].
• The inhibitory effect of L-histidine on METH-induced stereotyped behavior was significantly blocked by coadministration of pyrilamine and zolantidine, indicating that the effect is mediated through H1 and H2 receptors [6].
• Although the antagonistic effect of GBE on pyrilamine-induced spatial memory deficits was weak, a significant difference was observed with TE and WME [7].
• Among the classic H1-blockers used in this study: pyrilamine, diphenydramine, promethazine and chlorpheniramine, promethazine was the most effective and chlorpheniramine the least in inhibiting the active avoidance response; namely, a variation of prolongation in the response latency of the avoidance response [8].

High impact information on Pyranisamine

• The production of CTL-PA can take place in allogeneic mixed leukocyte cultures (MLC) treated with the drug pyrilamine, or when heat-inactivated stimulator cells are used [9].
• Finally, a histamine type 2 receptor antagonist (cimetidine) but not a type 1 receptor antagonist (mepyramine) blocked the induction of suppressor cells [10].
• (e) Pyrilamine (an H1 antagonist), but not metiamide (an H2 antagonist), blocked the effect of histamine on cGMP from which it is inferred that histamine causes accumulation of cGMP in umbilical artery via its interaction with H1 receptors [11].
• The mast cell stabilizer lodoxamide and the histamine 1 and 2 receptor antagonists pyrilamine and ranitidine, respectively, did not significantly alter NT-induced Isc increase [12].
• Histamine responses were blocked by the H1 antagonist mepyramine but were not altered by a diamine oxidase inhibitor [13].

Chemical compound and disease context of Pyranisamine

• Although the effects of pyrilamine, cromolyn, or aprepitant on ET-induced vascular leakage suggest a possible role for mast cells (MC) and sensory neurons in ET-induced edema, ET did not elicit degranulation of human skin MC or substance P release from NT2N cells in vitro [14].
• 5 Specific doses of atropine, mepyramine (H1-blocker) and methysergide (5-HT antagonist) did not modify the anaphylactic reaction in coronary arteries, suggesting a negligible role for these biogenic amines [15].
• Pretreatment with a precursor of HA, L-histidine (750mg/kg), significantly inhibited the METH (3 mg/kg)-induced stereotyped behavior, whereas pretreatment with an inhibitor of HA synthesis, alpha-fluoromethylhistidine (FMH) (100 mg/kg), an H1 antagonist pyrilamine (5 mg/kg) or an H2 antagonist zolantidine (5 mg/kg) enhanced it [6].
• 6. A combination of all three compounds (mepyramine, methysergide and montelukast) reduced ovalbumin-induced microvascular leakage in airway tissue to basal levels (70 - 78%) and almost completely inhibited bronchospasm (92%) [16].
• The delayed phase of the contraction which took several minutes to develop in both the mepyramine-treated lung strip and trachea was not due to prostaglandins E1, F2alpha or bradykinin, the probable mediator being slow reacting substance of anaphylaxis (SRS-A) [17].

Biological context of Pyranisamine

• All histamine-induced responses, including chemotaxis and DNA synthesis, are completely inhibited by the H1 receptor antagonist pyrilamine, but not by cimetidine, an inhibitor of histamine H2 type receptors [18].
• Chlorpheniramine and pyrilamine blocked IKr relatively weakly (IC50 = 1.6 and 1.1 mumol/L, respectively) and IKs and IK1 less than 20% at 10 mumol/L [19].
• Histamine H(1) receptor density was not altered by PCA surgery, whereas pyrilamine treatment led to the complete blockade of H(1) receptors in both sham- and PCA-operated rats [20].
• In contrast, pyrilamine increased the movement time and velocity in PCA-operated rats, particularly in the dark phase, and improved the precision of the circadian rhythms of locomotion and feeding [20].
• RESULTS: Inhalation of histamine caused a dose-dependent decrease in mucus score, an effect that was inhibited by pretreatment with the H2-receptor antagonist cimetidine but not with the H1-receptor antagonist mepyramine or the H3-receptor antagonist thioperamide [21].

Anatomical context of Pyranisamine

• (ii) Simultaneous administration of H1 and H2 histamine receptor antagonists (pyrilamine and famotidine, respectively) greatly diminishes recruitment and adhesion of both neutrophils (<20% of control) and monocytes/macrophages (<30% of control) to implants [22].
• The neurotoxin tetrodotoxin (100 micrograms/kg i.v.) abolished the depressor response to spinal cord stimulation, whereas treatment with propranolol (0.5 mg/kg per minute i.v.), atropine (0.05 mg/kg per minute i.v.), or a combination of pyrilamine (0.5 mg/kg per minute i.v.) and cimetidine (0.5 mg/kg per minute i.v.) did not affect the response [23].
• However, platelet-activating factor induces a slowly developing, sustained contractile wave in ileum that is not inhibited by an antihistaminic compound, pyrilamine, whereas C3a and C5a stimulate rapid transient contraction that is abrogated by the antihistamine [24].
• The antihistamine mepyramine, administered orally, inhibited vasopermeability but not basophil degranulation [25].
• Greater inhibition with pyrilamine was seen in IBD small intestine but its effect was less in IBD colon [26].

Associations of Pyranisamine with other chemical compounds

• The PAF receptor antagonist WEB 2086 (2 mg/kg i.v.), the H1 blocker pyrilamine (10 mg/kg i.v.), and leukocyte depletion with cyclophosphamide (150 mg/kg i.p.) completely abolished the PAF priming effect [27].
• Binding was competitively displaced by N alpha-MeHA (IC50 = 5.8 +/- 0.7 nM), (R) alpha-MeHA (IC50 = 9 +/- 1 nM), and thioperamide (IC50 = 85 +/- 10 nM), but not by famotidine (H2 antagonist) or by mepyramine (H1 antagonist) [28].
• Furthermore, the increase in total immunoreactive LTB in mepyramine-treated FFD animals was significantly greater than the increase in LTB4 in mepyramine-treated BFD guinea pigs at 2 to 8 min after antigen challenge (p less than 0.05) [29].
• Pretreatment with the H1 antagonist mepyramine and the H2 antagonist cimetidine caused a similar reduction in SP-induced PPE in main bronchi of both strains [30].
• A consequence of the slow dissociation at 4 degrees is that the IC50 for mepyramine inhibition of promethazine-sensitive [3H]mepyramine binding at 4 degrees is independent of the concentration of [3H]mepyramine if the cerebellar homogenate is first incubated with the nonradioactive antagonist before addition of the 3H-ligand [31].

Gene context of Pyranisamine

• IL-4 treatment increased the expression of mRNA for histamine receptor 1 (HR1) and shifted the inhibition curve for pyrilamine, a specific HR1 antagonist [32].
• 3. Neither atropine (0.1 microM) nor l-NOLA (100 microM), nor indomethacin (10 microM) alone or in combination with either ranitidine (10 microM) or mepyramine (10 microM), affected responses to SP [33].
• The action of NKA, NKB or SP was not significantly modified in presence of thiorphan (10 microM), atropine (1 microM), mepyramine (1 microM) or indomethacin (5 microM) [34].
• H1 receptor antagonist pyrilamine reversed the effect of histamine on STAT6 phosphorylation [35].
• In the presence of mepyramine, and H1 receptor antagonist, the effects of histamine and compound 48/80 were reversed to inhibition of both LES basal tension and EB off response amplitude, while the effect of PEA was abolished [36].

Analytical, diagnostic and therapeutic context of Pyranisamine

• (3) The depression by histamine of the contractions and the efflux of radioactive compounds caused by electric stimulation were inhibited by an H2-receptor antagonist (metiamide), but were unaffected by an H1-receptor antagonist (pyrilamine) [37].
• In clinical studies, diphenhydramine, hydroxyzine, orphenadrine and pyrilamine have been shown to produce analgesia as simple entities but chlorpheniramine has not and results with phenyltoloxamine have been equivocal when tested alone [38].
• Injectable aspirin and mepyramine abolish post-ischaemic hyperalgesia in rats [39].
• We have studied the characteristics of carbon-11 labeled pyrilamine as a radioligand for investigating histamine H1 receptors in human brain with positron emission tomography (PET) [40].
• The PEA-induced constriction was blocked by the histamine H1 antagonist, mepyramine [41].

References