Disease relevance of BQ 485

• In contrast, treatment of LPS-rats with BQ-485 augmented the hypotension (at 360 min), but did not affect the vascular hyporeactivity elicited by endotoxaemia [1].
• LP-Q plots were generated on separate days during normoxia and hypoxia (arterial PO(2) approximately 50 Torr) in the intact condition, after selective ET(A)-receptor inhibition (BQ-485), and after combined ET(A+B)-receptor inhibition (bosentan) [2].
• A novel endothelin ETA receptor antagonist, BQ-485, and its preventive effect on experimental cerebral vasospasm in dogs [3].
• We examined the preventive effect of a novel ETA receptor antagonist, BQ-485, on experimental vasospasm using canine two-hemorrhage model of subarachnoid hemorrhage [3].
• Effect of an endothelin-1 antagonist, BQ-485, on cerebral oxygen metabolism after complete global cerebral ischemia in dogs [4].

High impact information on BQ 485

• RESULTS: BQ-485 infusion had no significant effect on hepatic microcirculation and liver injury [5].
• The initial vasoconstriction appeared to be mediated by both ET(A) and ET(B) receptors, as judged by inhibitory effects of their antagonists, BQ-485 and BQ-788, respectively, while the late elevation of the resistance was not attenuated by these reagents, but rather enhanced by the ET(B) blockade [6].
• Coculture of BAECs and VSMCs enhanced both ET-1 and VEGF gene expression in these cells, and the conditioned media from BAECs and VSMCs reproduced the augmentation of each gene expression, which was partially inhibited by BQ-485 or an antibody specific to VEGF [7].
• Furthermore, coincubation with 20 nmol/L BQ-485, an antagonist of one type of endothelin receptor (ETA), prevented the enhancement of interleukin-1-induced cytotoxicity in cocultured vascular smooth muscle cells [8].
• The action of ET-1 was also inhibited by the selective ET(A) receptor antagonist BQ-485 (10(-7) M) [9].

Biological context of BQ 485

• Preincubation with BQ-485 (10(-6) M) or BQ-123 (3 x 10(-6)) (ET(A)-receptor antagonist) significantly augmented the ET-1-induced vasodilatation in control mesenteric arterial beds, but not that in beds from diabetic rats [10].
• The IC50 value of BQ-485 on [125I]endothelin-1 binding was 3.4 x 10(-9) M for ETA receptor and 26 x 10(-6) M for ETB receptor [3].
• Since NO inhibits ET production in the endothelium, we speculated that the increase in MAP-RSNA slope was due partly to an unmasking of ET, and thus recorded MAP, heart rate, and RSNA during intravenous infusions of both L-NMMA and the ET-type-A-receptor antagonist BQ-485 (0.10 mg/kg/min) [11].
• Endothelin-A receptor antagonist BQ-485 protects against intraocular pressure spike induced by laser trabeculoplasty in the rabbit [12].

Anatomical context of BQ 485

• The I/R-induced increases in mucosal permeability and polymorphonuclear leukocyte (PMN) infiltration were significantly attenuated by pretreatments with ET(A) (BQ-485) and/or ET(B) (BQ-788) receptor antagonists [13].
• BQ-485 was given directly into the carotid artery at 0.03 mg/kg per min for 30 min, starting 15 min after reperfusion in the treatment group (n = 5) [4].
• To evaluate the effects of the newly synthesized ETA receptor-selective antagonist, BQ-485 (N-perhydroazepin-l-ylcarbonyl-Leu-D-Trp-D-Trp-OH), on the cerebral metabolism of oxygen during the delayed cerebral hypoperfusion that follows global cerebral ischemia, we occluded the ascending aorta and caval veins of 10 beagle dogs for 12.5 min [4].
• METHODS: Under general anaesthesia, 10 microl of 10(-5) M BQ-485 was injected into the anterior chamber of the right eye, and 10 microl of balanced salt solution (BSS) into the contralateral anterior chamber, for 12 pigmented rabbits [12].

Associations of BQ 485 with other chemical compounds

• These results suggest that both BQ-485 and BQ-518 principally share the cMOAT transporter with BQ-123 [14].

Gene context of BQ 485

• Moreover, the action of ET-3 was also blocked by BQ-485 (10(-7) M) [9].
• ET-1 increased 3H-leucine incorporation and beta-MyHC promoter activities, which were blocked by the specific ET(A) receptor antagonist BQ-485 [15].
• Diameters of mucosal vessels and blood flow were increased significantly by endothelin-A receptor antagonist (BQ-485) in the portal hypertensive rats [16].
• BQ-485 (ET(A) receptor antagonist; 2 mg/kg, subcutaneously) also abolished ammonia-induced lesions and gastric immunoreactive TRH changes [17].

References