High impact information on Ici-192605

• Only 8-iso-PGE(2) was able to evoke substantial contractions in the presence of ICI 192605 and only in the pulmonary vein [1].
• 4. The contraction of MA to H(2)O(2) (5 x 10(-4) M) was greatly inhibited by SQ 29548 and ICI 192605 (thromboxane A(2) (TXA(2))/prostaglandin H(2) receptor antagonists), quinacrine (a phospholipase A(2) (PLA(2)) inhibitor), indomethacin and diclofenac (cyclooxygenase (COX) inhibitors), and furegrelate (a TXA(2) synthase inhibitor) [2].
• 4. In the presence of ICI 192605 (10(-6) M), 8-iso PGE(1) evoked modest dose-dependent relaxations in human and canine pulmonary vein, and in canine pulmonary artery, but not in the human pulmonary artery [3].
• We tested the hypothesis that inhaled prostaglandin (PG) D2-induced bronchoconstriction is mediated by interacting with the TP receptor antagonist, ICI 192605, on the bronchoconstrictor response to inhaled PGD2 in a double-blind, placebo-controlled and crossed-over trial in normal subjects [4].
• However, in the presence of N(G)-nitro-L-arginine (3 x 10(-5) M, a nitric oxide synthase inhibitor), Ro 68070 (10(-4) M, a thromboxane synthetase inhibitor-thromboxane A2/prostaglandin H2 receptor antagonist) or ICI 192605 (10(-5) M, a thromboxane A2 receptor antagonist) the relaxant response to L-carnitine was significantly inhibited [5].

Anatomical context of Ici-192605

• A number of eicosanoids caused plasma membrane blebbing in hepatocytes and this could be inhibited in a dose-dependent fashion by the receptor antagonists AH6809 and ICI 192605 [6].

Associations of Ici-192605 with other chemical compounds

• ICI 192605 significantly shifted the dose-response curve to inhaled PGD2 to the right by a median of 3.4 fold (Wilcoxon rank sign test, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)[4]

References