Disease relevance of Lilly 04432

• 2. While hypoxia induced a high incidence of ventricular tachycardia or fibrillation, only a few preparations developed ventricular arrhythmias in response to perfusion with high concentration of histamine, 2-pyridylethylamine or impromidine [1].
• The technique is based on the inhibition of the tachycardia caused by intravenous administration of the H1-receptor agonist, 2-pyridylethylamine [2].

High impact information on Lilly 04432

• In addition, the H1 agonist 2-pyridylethylamine, but not the H2 agonist dimaprit, contracted mesangial cells [3].
• In coronary artery cells, 100 microM 2-(2-aminoethyl)pyridine (an H1 receptor agonist) or 10 microM ryanodine, agents that cause an increase in [Ca2+]i, also caused a significant reduction of the 4-AP-sensitive IK(dr) similar to that produced by Mg2+ [4].
• Thus, dithiothreitol increased the maximal accumulation of [3H]inositol phosphates produced by both 2-pyridylethylamine and 2-methylhistamine, which appeared to act as partial agonists in guinea-pig cerebral cortex [5].
• In the presence of DTT the partial H1-receptor agonist 2-pyridylethylamine (100 microM) increased [Ca2+]i from 112 +/- 14 nM to 237 +/- 24 nM (N = 10) [6].
• 2-Methylhistamine (2-MH), 2-pyridylethylamine (PEA) and 4-methylhistamine (4-MH) produced similar sustained contractions of the muscularis mucosae [7].

Biological context of Lilly 04432

• An H2-receptor agonist, 4-methylhistamine and an H1-receptor agonist, 2-(2-pyridyl)ethylamine, both produced vasodilatation which was blocked by metiamide and mepyramine, respectively [8].
• The H1 receptor agonist, 2-pyridylethylamine (PEA) (10(-9)-10(-3) M), induced concentration-dependent relaxation in precontracted rings and provoked vasoconstriction at basal tone [9].

Anatomical context of Lilly 04432

• 2 The trachea contracted (isometric) to histamine, 2-pyridylethylamine (2-PEA), acetylcholine and K+ but no response to histamine H2-receptor agonists were observed [10].
• In the present study we have investigated the cardiac effects of histamine, 4-methylhistamine (a specific H2-receptor agonist) and 2-pyridylethylamine PEA, a specific H1-receptor agonist] on spontaneously beating right atria and electrically driven left atria and right ventricle strips of the guinea pig [11].
• Of particular interest, gel filtration of supernatants generated by stimulating mononuclear cells with either histamine, dimaprit (but not 2-pyridylethylamine), concanavalin A, or candida albicans resulted in similar elution profiles with regard to inhibition of lymphocyte proliferation [12].
• This study further confirms that the derivatives made of a 2-(2'-aminoethyl)pyridine ligand displayed superior activity against the cell lines particularly when the connecting arm is 8-10 carbon atoms long [13].
• Histamine, 2-(2-pyridyl)ethylamine (PEA), a specific H1 receptor agonist, and 4-methylhistamine (4-MH), a specific H2 receptor agonist, produced a dose-dependent contraction of estrogen-primed guinea pig uterus and taenia coli [14].

Associations of Lilly 04432 with other chemical compounds

• SK&F 93319 was an effective antagonist of histamine, 2-(2-aminoethyl)pyridine or dimaprit-induced vasodilatation in femoral and gastric vasculature [15].
• These antagonists abolished or significantly attenuated the corticosterone response to 2-pyridylethylamine (PEA), an H1-receptor agonist, and to dimaprit and 4-methylhistamine(4-MeHA), H2-receptor agonists [16].
• The increase in working memory errors induced by intrahippocampal 32 microg/side pyrilamine was significantly reduced by concurrent infusion of the histamine H1 receptor agonist 2-pyridylethylamine (3.2 and 10 microg/side) [17].
• On the other hand, highly selective histamine H2 receptor agonist dimaprit mimicked the excitatory effect of histamine on the GP neurons (n = 23), while histamine H1 receptor agonists, including 2-pyridylethylamine (n = 22), 2-thiazolyethylamine (n = 9) and betahistine (n = 9), did not cause GP neurons any response [18].

Gene context of Lilly 04432

• The H1 receptor agonist 2-pyridylethylamine induced a biphasic response: contraction followed by dilation [19].
• The histamine H1 receptor agonist 2-pyridylethylamine induced sneezing and nasal rubbing in a dose-dependent-manner in wild-type mice, but no such increase was found in histamine H1 receptor-deficient mice [20].
• A similar effect was obtained with 2-pyridylethylamine, a histamine H1-receptor agonist [21].
• The histamine H2 receptor agonists dimaprit and 4-methylhistamine, but not the H1 receptor agonists 2-pyridylethylamine, aminoethylthiazole and 2-methylhistamine, modulated the IL-1 production in a similar manner to histamine [22].
• The H1-histamine agonist, 2-(2-pyridyl)ethylamine (PEA) in high doses released prolactin and its effect was partially prevented by metiamide [23].

Analytical, diagnostic and therapeutic context of Lilly 04432

• Intradermal injection of histamine, 2-pyridylethylamine (a selective H1-agonist), and dimaprit (a selective H2-agonist) dose-dependently induced the wheal response in squirrel monkeys and guinea pigs, although the reaction to dimaprit was much weaker than that to the other agonists [24].

References