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1 n ACE inhibitor but not by an angiotensin II AT1 receptor antagonist.
2  receptor antagonist but not by losartan, an AT1 receptor antagonist.
3 ry circulation in DCM that are not shared by AT1 receptor antagonists.
4 rs compared with newly available angiotensin AT1 receptor antagonists.
5 to the potential therapeutic implications of AT1 receptor antagonists.
6 bitor but not with an angiotensin II type 1 (AT1) receptor antagonist.
7 -4) mol/l losartan, a type 1 angiotensin II (AT1) receptor antagonist.
8 converting enzyme inhibitor, or losartan, an AT1 receptor antagonist, abolished both drinking and Fos
9  Ca2+ by AT1-AAs was blocked by losartan, an AT1 receptor antagonist, and by a 7-amino-acid peptide t
10                                 Losartan, an AT1 receptor antagonist, and inhibitors of either mitoge
11 eatment protocol: (1) candesartan cilexetil (AT1 receptor antagonist) at 1 mg/kg body wt per d; (2) c
12 hese responses were inhibited by PD98059 and AT1 receptor antagonist candesartan.
13 was completely inhibited by co-infusion with AT1 receptor antagonist, candesartan.
14 inea pig hearts treated with BILA2157 or the AT1 receptor antagonist EXP3174.
15 ravenous injection of angiotensin II type 1 (AT1) receptor antagonist improves the baroreceptor refle
16 an (10 mg kg-1, I.V.), the angiotensin (AII) AT1 receptor antagonist, induced a fall in MABP (115 +/-
17                        Valsartan, a specific AT1 receptor antagonist inhibited Ang II binding, wherea
18 antagonist PD 123319 (1 mumol/L) but not the AT1 receptor antagonist losartan (1 mumol/L) blocked the
19                      Coadministration of the AT1 receptor antagonist losartan (1 to 1000 ng) elicited
20                                          The AT1 receptor antagonist losartan (2 microm, n = 6) aboli
21               Concomitant treatment with the AT1 receptor antagonist losartan (5 to 25 mg.kg-1.d-1) d
22 evoked Icat1 and Icat2 were inhibited by the AT1 receptor antagonist losartan and the phospholipase C
23          The vasodilator hydralazine and the AT1 receptor antagonist losartan had comparable effects
24             The MMP inhibitor GM6001 and the AT1 receptor antagonist Losartan inhibited these effects
25                                          The AT1 receptor antagonist losartan normalized blood pressu
26 25I]Sar1-Ang II binding was displaced by the AT1 receptor antagonist losartan, indicating the presenc
27 el Ca2+-dependent pathway was blocked by the AT1 receptor antagonist losartan, or by including guanos
28  AT2 receptor antagonist PD 123319 (PD), the AT1 receptor antagonist Losartan, the nitric oxide synth
29    The effect of Ang II was abolished by the AT1 receptor antagonist losartan.
30 T2 receptor binding were determined with the AT1 receptor antagonist losartan.
31  mRNA accumulation that was prevented by the AT1 receptor antagonist losartan.
32 etched hearts with the specific angiotensin (AT1) receptor antagonist losartan abolished stretch-medi
33 ablated by treatment with the Ang II type 1 (AT1) receptor antagonist losartan.
34 istration of angiotensin II receptor type 1 (AT1) receptor antagonists losartan or EXP-3174 simultane
35                             Inhibition by an AT1 receptor antagonist (losartan metabolite: E3174) or
36              Pretreatment of the SFO with an AT1 receptor antagonist, losartan (1 microgram/200 nl),
37  (p < 0.01), and was inhibited by a specific AT1 receptor antagonist, Losartan (74 +/- 14%).
38                         Administration of an AT1 receptor antagonist, losartan, also significantly in
39 onse by Ang II was completely blocked by the AT1 receptor antagonist, losartan.
40 etermined by the sensitivity of Jprox to the AT1 receptor antagonist, losartan.
41 th reflexes were blocked by an ANGII type 1 (AT1) receptor antagonist, losartan (20 microM).
42  assessed the role of angiotensin II type 1 (AT1) receptor antagonists on inflammatory mechanisms inv
43 ffects of intravenous injection of CV-11974 (AT1 receptor antagonist) on the baroreflex control of re
44 malized to 100% ANG II effect in each group, AT1 receptor antagonists produced the same degree of blo
45 p38MAPK and JNK by AngII was inhibited by an AT1 receptor antagonist, RNH6270 and EGF markedly activa
46                Inhibition of the response by AT1 receptor antagonist suggests mediation by the AT1B r
47                        Administration of the AT1 receptor antagonist telmisartan 1 hour post-injury s
48 otensin-converting enzyme inhibitors and the AT1 receptor antagonists, unblocked aldosterone levels r
49 is effect was AT1 receptor mediated, because AT1 receptor antagonists valsartan, candesartan, and los