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1 and osteoblastic metastases in vivo via the endothelin A receptor.
2 eases PKC activity via binding to endogenous endothelin(A) receptors.
5 ety of zibotentan (ZD4054), an oral specific endothelin A receptor antagonist, has been investigated
8 209,670, and the less potent, but selective, endothelin-A receptor antagonist BMS-182,874 in radiocon
9 -phenyl-4H-1-benzopyran-4-one (LY294002) and endothelin-A receptor antagonist cyclo(L-Leu-D-Trp-D-Asp
10 with a highly selective, well-characterized endothelin-A receptor antagonist partly protected GFR, a
12 Half of the rings were pretreated with the endothelin-A receptor antagonist, BQ123 (10(-5) M or 10(
14 gations involving alpha-emitting radium-223, endothelin-A receptor antagonists atrasentan and ziboten
15 ishment of osteoblastic bone metastases, and endothelin A receptor blockade represents effective trea
19 riction, which was reversed partially by the endothelin A receptor blocker BQ123 and completely by fa
20 experiments, endothelin 1 (which stimulates endothelin A receptors) caused comparable contraction of
21 dothelin signaling via the activation of the endothelin-A receptor (EDNRA) by endothelin-1 may play a
22 helin-1 (Edn1)-induced signaling through the endothelin-A receptor (Ednra) is crucial for cranial NCC
25 tions mediated by two receptor subtypes, the endothelin A receptor (ET(A)R) and the endothelin B rece
26 amined the effect of atrasentan, a selective endothelin A receptor (ET(A)R) antagonist, on albuminuri
28 othelins stimulate leptin production via the endothelin-A receptor (ET(A)), as judged by a potency ra
29 can produce ET-1, undergo ET-1-dependent and endothelin-A receptor (ET(A))-dependent activation, and
31 o three groups: placebo (RVD+PTRAS), chronic endothelin-A receptor (ET-A) blockade (RVD+PTRAS+ET-A),
33 g-term treatment strategy with the selective endothelin-A receptor (ETA) antagonist, ambrisentan, des
34 angiotensin II type 1A receptor (AT1AR) and endothelin A receptor (ETAR), activation of ETARs result
39 eviously showed that activation of the human endothelin A receptor (HETAR) by endothelin-1 (Et-1) sel
42 ults are consistent with the hypothesis that endothelin-A receptors mediate endothelin-induced change
43 sed in rejecting allotransplanted lungs, (3) endothelin-A receptors mediate the proliferative respons
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