ライフサイエンスコーパス: endothelin A receptor

1 and osteoblastic metastases in vivo via the endothelin A receptor.

2 eases PKC activity via binding to endogenous endothelin(A) receptors.

3 Therefore, we assessed the effect of endothelin-A receptor antagonism in the response of pulm

4 between treatment with placebo and selective endothelin-A receptor antagonism.

5 2 diabetes using a low dose of the selective endothelin A receptor antagonist atrasentan reduces albu

6 Treatment with an orally active endothelin A receptor antagonist dramatically decreased

7 ety of zibotentan (ZD4054), an oral specific endothelin A receptor antagonist, has been investigated

8 Atrasentan, a selective endothelin A receptor antagonist, has been shown to redu

9 BQ123, an endothelin A receptor antagonist, prevented thrombin's i

10 209,670, and the less potent, but selective, endothelin-A receptor antagonist BMS-182,874 in radiocon

11 -phenyl-4H-1-benzopyran-4-one (LY294002) and endothelin-A receptor antagonist cyclo(L-Leu-D-Trp-D-Asp

12 with a highly selective, well-characterized endothelin-A receptor antagonist partly protected GFR, a

13 The endothelin-A receptor antagonist, BQ-123, could attenuat

14 Half of the rings were pretreated with the endothelin-A receptor antagonist, BQ123 (10(-5) M or 10(

15 chronic kidney disease, SGLT2 inhibitors and endothelin A receptor antagonists (ERAs) can reduce albu

16 Interest has grown in using Endothelin A receptor antagonists as adjuvant or combina

17 gations involving alpha-emitting radium-223, endothelin-A receptor antagonists atrasentan and ziboten

18 ishment of osteoblastic bone metastases, and endothelin A receptor blockade represents effective trea

19 Acute endothelin A receptor blockade with FR-139317 resulted i

20 Endothelin-A receptor blockade is an effective means of

21 In summary, endothelin-A receptor blockade with a highly selective,

22 riction, which was reversed partially by the endothelin A receptor blocker BQ123 and completely by fa

23 experiments, endothelin 1 (which stimulates endothelin A receptors) caused comparable contraction of

24 dothelin signaling via the activation of the endothelin-A receptor (EDNRA) by endothelin-1 may play a

25 helin-1 (Edn1)-induced signaling through the endothelin-A receptor (Ednra) is crucial for cranial NCC

26 Endothelin-A receptor (Ednra) signaling in crest cells i

27 cranial NCCs, some of which are regulated by endothelin-A receptor (Ednra) signaling.

28 tions mediated by two receptor subtypes, the endothelin A receptor (ET(A)R) and the endothelin B rece

29 amined the effect of atrasentan, a selective endothelin A receptor (ET(A)R) antagonist, on albuminuri

30 mice following treatment with the selective endothelin A receptor (ET(A)R) blocker, atrasentan.

31 uring ischaemia through direct activation of endothelin A receptors (ET(A)Rs).

32 othelins stimulate leptin production via the endothelin-A receptor (ET(A)), as judged by a potency ra

33 can produce ET-1, undergo ET-1-dependent and endothelin-A receptor (ET(A))-dependent activation, and

34 Activation of endothelin-A receptor (ET(A)R) by endothelin-1 (ET-1) dr

35 o three groups: placebo (RVD+PTRAS), chronic endothelin-A receptor (ET-A) blockade (RVD+PTRAS+ET-A),

36 ly identical to the defects seen in ET-1 and endothelin A receptor (ETA)-deficient embryos.

37 g-term treatment strategy with the selective endothelin-A receptor (ETA) antagonist, ambrisentan, des

38 angiotensin II type 1A receptor (AT1AR) and endothelin A receptor (ETAR), activation of ETARs result

39 Mechanistically, endothelin A receptor (ETAR)-positive macrophages are hi

40 on of its cognate G protein-coupled receptor endothelin A receptor (ETAR).

41 In EOC, the endothelin-1 (ET-1, EDN1)-endothelin A receptor (ETAR, EDNRA) signaling axis regul

42 Mice with a null mutation in endothelin A receptor gene (ET(A)) or in the gene of its

43 eviously showed that activation of the human endothelin A receptor (HETAR) by endothelin-1 (Et-1) sel

44 ion of similar magnitude (P </= 0.05) of the endothelin A receptor in the lung tissue.

45 Selectively inhibiting the endothelin A receptors in dogs with CHF produced hemodyn

46 d with biomechanical strain, which activates endothelin-A receptors leading to mesangial filopodia fo

47 ults are consistent with the hypothesis that endothelin-A receptors mediate endothelin-induced change

48 sed in rejecting allotransplanted lungs, (3) endothelin-A receptors mediate the proliferative respons

49 No change in expression of endothelin A receptor was observed 7 days after inductio

50 This effect, mediated by the endothelin-A receptor, was associated with a shift in ML