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1 e stable hydrolysis product of prostacyclin (prostaglandin I2).
2 lthough continuous infusion of prostacyclin (prostaglandin I2, a potent vasodilator released by vascu
5 ptor antagonists, indicating a role for both prostaglandin I2 and E2 Activation of ERKs and p38, but
6 endothelial cells depressed biosynthesis of prostaglandin I2 and prostaglandin E2, elevated blood pr
7 ein kinases triggers the rapid production of prostaglandins I2 and E2 through cyclooxygenase (COX)-1
9 e endothelium of the antithrombotic mediator prostaglandin I2 as a result of inhibition of endothelia
10 production of the counteracting eicosanoids prostaglandin I2, E1, E2, and A2, while in HRGEC only mo
11 vo effects of pharmacological agonism of the prostaglandin I2 (IP) receptor in pancreatic beta-cells
12 of sacrifice revealed significantly elevated prostaglandin I2 levels in the transgenic animals, coupl
15 f 6-keto-PGF1alpha, the stable metabolite of prostaglandin I2 (PGI2) and thromboxane B2 (TXB2), the s
16 dered resistant to activation by exposure to prostaglandin I2 (PGI2) or forskolin, both of which incr
17 , it remains unknown whether prostacyclin or prostaglandin I2 (PGI2) plays a significant role in modu
19 so observed enhanced autocrine production of prostaglandin I2 (PGI2, also called prostacyclin) in Cav
25 showed reduced, but not absent, formation of prostaglandin I2 (prostacyclin; control 956 +/- 422 pg/m
26 P4 prostaglandin E2 (PGE2) receptors and the prostaglandin I2 receptor were changed in these cells by
27 xane A2 receptor, prostaglandin D2 receptor, prostaglandin I2 receptor, and one of the PGE2 (EP1) rec
28 ceptor (TP) (11) while sparing EP2, EP3, and prostaglandin I2 receptors (IPs); Kb values (in nanomole
29 s determined by experiments with inhibitors [prostaglandin I2, staurosporine, wortmannin, the endothe
30 ds: prostaglandin E2, prostaglandin F2alpha, prostaglandin I2, thromboxane A2, and prostaglandin D2.
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