Disease relevance of BE-2254

• BE 2254 could not block ischemic preconditioning (3.9 +/- 1.1% infarction, P < .01 vs control value) [1].
• 2. Heat production (kJ/kg body-weight (W)0.75 per d) was increased by 23% in rats fed on the MP diet ad lib., as compared with their HP controls (P less than 0.01) [2].
• 2. Heat exposure of laying fowl resulted in a 1.1 degree C rise in body temperature, a 10-fold increase in respiration frequency and mild hypocapnia and hypoxaemia [3].

Psychiatry related information on BE-2254

• A lack of spatial working memory deficits in BE 2254 or saline-injected animals was also observed in two other conditions of the behavioral protocol [4].

High impact information on BE-2254

• Phentolamine and the aqueous soluble alpha 1-adrenergic antagonist BE-2254 administered as late as 2 min before reperfusion similarly attenuated the increase in tissue calcium [5].
• Epinephrine at a concentration of 10(-6) M also initiated triggered activity in Purkinje fibers exposed to LPC (75 microM), a response blocked by l-propranolol (2 X 10(-7) M and 10(-6) M) but not by the alpha 1-adrenergic blocking agent BE-2254 (10(-6) M) [6].
• Rauwolscine (10(-9), 10(-8), and 10(-7) mol/liter) and BE 2254 (10(-7) but not 10(-8) mol/liter) significantly enhanced stimulation-induced tritium efflux in arteries and veins [7].
• Heart rate, arterial pressure, femoral flow, and femoral resistance responses elicited from efferent spinal pathways were significantly attenuated following superfusion of the spinal cord with the alpha-antagonists BE-2254 (HEAT) and phentolamine [8].
• 125I-Labeled BE 2254 (125IBE) was found to bind rapidly and reversibly to a single class of high-affinity binding sites in homogenates of rat vas deferens [9].

Biological context of BE-2254

• 2. Heat stress increased body temperature (Tb) and respiration rate (RR) but both were higher in birds given CW after 4 and 5 h than in TW-infused controls [10].
• 2. Heat production rose with increase in food intake and environmental temperature [11].
• The antagonist effects of BE 2254 against TL 99-induced vasoconstriction was not altered by these pretreatments [12].

Anatomical context of BE-2254

• The effects of 2-[beta-(4-hydroxyphenyl)-ethyl-aminomethyl]-tetralone (BE 2254) on pre- and postsynaptic alpha-adrenoceptors were studies in isolated rabbit hearts and strips of rabbit pulmonary arteries [13].
• In particular, alpha 1-adrenoceptor-selective antagonists (prazosin, WB 4101, BE 2254...) displaced with nanomolar affinity about 15 and 40% of the specific [3H]ketanserin binding in human and pig frontal cortex membranes, respectively [14].
• To this end, C57Bl/6 mice were infused bilaterally into the lateral septal nuclei with 500 ng/0.2 microliter of BE 2254, a selective alpha 1 postsynaptic adrenoceptor antagonist [4].
• (2) Heat shock and hyperosmolarity increase expression of differentiation markers in K562, HT29, HL60 and in K562, PANC1, and HT29 cells, respectively [15].
• Dopamine (5.3 X 10(-6) to 5.3 X 10(-5) M) decreased the force of spontaneous myogenic contractions of the rat portal vein in a concentration-dependent manner in the presence of the alpha-adrenoreceptor antagonist BE-2254 [16].

Associations of BE-2254 with other chemical compounds

• In superfused pulmonary arteries, BE 2254 produced a parallel shift to the right of the concentration-response curve for noradrenaline: increasing effect on tension, pA2 = 8.75 [13].
• 4 In the transmurally stimulated guinea-pig ileum, BE 2254 was a potent antagonist of TL99, or clonidine-induced inhibition of the twitch response (presynaptic alpha 2-adrenoreceptor effects), but did not antagonize the effects of morphine [12].
• The potency of BE 2254 against NA-induced vasoconstriction was markedly reduced by pretreatment with prazosin and propranolol [12].
• 2 BE 2254 was a competitive and potent antagonist of NA, Phenylephrine (PE) or stimulation-induced vasoconstriction in the pithed rat, but only exerted a weak antagonism of postsynaptic alpha 2-adrenoreceptor vasoconstriction induced by N,N-diMe-6,7-diOHATN (TL 99) or azepexole (BHT 933) [12].

Gene context of BE-2254

• Contribution of heat transfer to turbine blades and vanes for high temperature industrial gas turbines. Part 2: Heat transfer on serpentine flow passage [17].

Analytical, diagnostic and therapeutic context of BE-2254

• Transmural electrical stimulation of BIAA segments resulted in activation of ERK, which was inhibited by the alpha(1)-AR-selective antagonist BE 2254 (2-[[beta-(4-hydroxyphenyl)ethyl]aminomethyl]-1-tetralone) [18].
• Rapid and simple purification of the 125I-labeled alpha-1 adrenergic radioligand 2-[beta-(4-hydroxylphenylethyl)aminomethyl] tetralone (BE 2254) using reversed-phase high-performance liquid chromatography [19].
• In these conditions, the BE 2254, as well as the saline-injected control group, showed an elevation of the anxiety level that may be the indirect expression of a nonspecific septal dysfunction induced by the vehicle injection rather than the normal behavioral response produced by the decrease of septal NA activity [4].
• 2. Heat treatment of the partial denture alloys tested resulted in reductions in strength, while the elongations varied [20].

References