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1 mouse fetal VSMCs, which express endogenous AT2 receptor.
2 effects are partly due to activation of the AT2 receptor.
3 ugh stimulation by Ang II at the angiotensin AT2 receptor.
4 apoptosis and abolished the up-regulation of AT2 receptor.
5 lpha2 and Gialpha3, also co-immunoselect the AT2 receptor.
6 f sodium restriction occur via ANG II at the AT2 receptor.
7 acid (AA) release from cultured neurons via AT2 receptors.
8 olved in this process other than the RAS and AT2 receptors.
9 ptor and activate the angiotensin II type 2 (AT2) receptor.
10 cells induced by the angiotensin II type 2 (AT2) receptor.
11 ossess abundant LOX-1 as well as Ang II (AT1>AT2) receptors, (2) Ang II upregulates LOX-1 receptor an
19 he target organ, exogenous administration of AT2 receptor agonists or angiotensin 1-7 analogs may sim
21 sibility that selective interactions between AT2 receptor and different G proteins may result in spec
22 he AT1-ant is triggered by activation of the AT2 receptor and is also mediated in part by kinins.
25 r olive reduced [125I]Sar1-Ang II binding to AT2 receptors and AT2 receptor mRNA levels in this area
27 contain many angiotensin II (Ang II) type 2 (AT2) receptors, and we previously determined that activa
28 ctivation was also inhibited by PD123319, an AT2 receptor antagonist but not by losartan, an AT1 rece
31 P in response to intravenous infusion of the AT2 receptor antagonist PD 123319 (PD), the AT1 receptor
37 lthough a pharmacological approach using the AT2 receptor antagonist PD123319 has implicated a role.
39 response, the effects of the central AT1 and AT2 receptor antagonists losartan and PD123319 were inve
40 CCDs with losartan but not PD123319 AT1 and AT2 receptor antagonists, respectively, blocked the resp
42 ese corresponding domains in the AT1 and the AT2 receptors are crucial to the activation mechanism, d
44 first use RT-PCR to show that AT1A, AT1B and AT2 receptors are expressed in thoracic spinal cord of t
45 ceptor blocker PD123319, indicating that the AT2 receptors are functional and exert an antigrowth eff
48 etic intracellular third loop peptide of the AT2 receptor (AT2-3LP, 22 amino acids) and control pepti
52 In the vasculature, the angiotensin type 2 (AT2) receptor (AT2R) exerts antiproliferative, antifibro
55 s after serum removal; instead, it increased AT2 receptor binding and enhanced angiotensin II-mediate
57 a by 50%, and produced a similar decrease in AT2 receptor binding in the molecular layer of the cereb
61 , functioning via the angiotensin II type 2 (AT2) receptor, blocked both the nicotine-induced activat
64 Ang II (100 nmol/L), in the presence of the AT2 receptor blocker PD123,319, elicited an inhibition o
65 VSMC (embryonic day 20) was increased by the AT2 receptor blocker PD123319, indicating that the AT2 r
66 with the AT1 receptor blocker, Losartan, the AT2 receptor blocker, PD 123319 (PD), or angiotensin II,
72 Taken together, our results suggest that AT2 receptor can crosstalk negatively with multiple fami
73 port that the stimulation of AT2 receptor in AT2 receptor cDNA-transfected rat adult vascular smooth
74 n the other hand, the angiotensin II type 2 (AT2) receptor counteracts the AT1 receptor-mediated tyro
78 altered in AT1A receptor-deficient mice, and AT2 receptor deficiency had no effect on lesion area or
82 by the activation of AT1 receptors, and that AT2 receptors do not appear to modulate hemodynamic resp
83 mouse are mediated by AT1 receptors and that AT2 receptors do not modulate the pressor response to An
84 n Agtr1a-/-; Agtr1b-/- mice, indicating that AT2 receptor does not exert acute depressor effects in t
86 is and that increased IRF-1 up-regulates the AT2 receptor expression after serum starvation, resultin
89 g were harvested to measure cortical AT1 and AT2 receptor expression, 125I-Ang II glomerular binding,
98 tibodies were both able to co-immunoselected AT2 receptor-Gialpha complexes, but consistent with the
99 Recently growth-inhibitory effects of the AT2 receptor have been reported to be mediated by the ac
102 mouse strain mutant for angiotensin type 2 (AT2) receptors have given new insight into this mystery.
103 ent study, we report that the stimulation of AT2 receptor in AT2 receptor cDNA-transfected rat adult
106 e present study was to determine the role of AT2 receptors in AngII-induced AAAs using a combination
108 in-converting enzyme, and the Ang II AT1 and AT2 receptors in embryonic day 10.25 Sprague-Dawley rats
112 To determine the roles of brain AT1 and AT2 receptors in this response, the effects of the centr
114 usly shown that angiotensin II (Ang II), via AT2 receptors, increases whole-cell K+ current in cultur
121 re, the potential biological significance of AT2 receptor-induced effects on both the nicotine-induce
122 mechanism of angiotensin II (Ang II) type 2 (AT2) receptor-induced apoptosis in PC12W (rat pheochromo
123 16-residue segment (Cys101-Val116) from the AT2 receptor induces constitutive activity, although Asn
124 trate that in PC12W cells the stimulation of AT2 receptor induces the activation of de novo pathway,
130 t the intracellular third loop domain of the AT2 receptor is closely linked with the cellular signali
136 The expression of the angiotensin II type 2 (AT2) receptor is developmentally and growth regulated.
137 third loop domain of angiotensin II type-2 (AT2) receptor is essential for the subsequent intracellu
142 doses of the angiotensin II receptor type 2 (AT2) receptor ligand CGP-42112 had only a weak inhibitor
143 othesize that this apoptotic function of the AT2 receptor may play an important role in developmental
150 de to MAP kinase phosphatase 1 inhibited the AT2 receptor-mediated MAP kinase dephosphorylation and b
152 d LO metabolite intracellular pathway in the AT2 receptor-mediated stimulation of neuronal IK by Ang
154 s AT1 receptor-mediated vasoconstriction and AT2 receptor-mediated vasodilation of coronary arteriole
155 tensin II (Ang II) elicits an Ang II type 2 (AT2) receptor-mediated increase in delayed-rectifier K+
157 These results suggest that activation of AT2 receptors modulates rat hypothalamus and brain stern
161 25I]Sar1-Ang II binding to AT2 receptors and AT2 receptor mRNA levels in this area by 50%, and produc
162 ously detected AT2 receptor binding, but not AT2 receptor mRNA, in the molecular layer of the cerebel
167 ion but attenuated the inhibitory effects of AT2 receptor on MAP kinase, Bcl-2 phosphorylation, and a
168 These results strongly suggest that the AT2 receptor plays a counterregulatory protective role m
169 eath and that angiotensin acting through the AT2 receptor protects dopamine neurons from rotenone tox
172 erved in the AT2 receptor; the corresponding AT2 receptor residues are, in fact, disruptive of AngII-
173 an and PD123,319 to block the Ang II AT1 and AT2 receptors resulted in reduced ventricular developmen
175 ein tyrosine phosphatases (PTPases) and that AT2 receptor stimulation is associated with a rapid acti
177 l mechanisms by which angiotensin subtype-2 (AT2) receptor stimulation induces net fluid absorption a
182 ins II or III, as documented for the AT1 and AT2 receptor subtypes, and is heavily distributed in the
183 II has a second receptor, the Ang II type 2 (AT2) receptor, the function of which, even after over 20
184 y of these residues are not conserved in the AT2 receptor; the corresponding AT2 receptor residues ar
185 ARB may exert antifibrotic actions via the AT2 receptor, through increased levels of angiotensin II
186 zed that angiotensin II (Ang II) acts at the AT2 receptor to stimulate renal production of nitric oxi
187 as used to inhibit 125I-SI Ang II binding to AT2 receptors to determine AT1 receptor density in brain
188 est that ANG II acts at the serosal side via AT2 receptors to stimulate cGMP production via soluble g
189 removal mediated apoptosis and up-regulated AT2 receptor, we transfected antisense oligonucleotides
191 eventh transmembrane-spanning domains of the AT2 receptor were substituted into the AT1 receptor were
192 ptapeptide metabolite Ang-(1-7), and AT1 and AT2 receptors were localized by immunohistochemistry and
194 rly, levels of the AT1 receptor, but not the AT2 receptor, were significantly lower in mesangial cell
195 giotensins; these angiotensins stimulate the AT2 receptor, which in turn may play an important role i
198 k2 activities was potentiated by blockade of AT2 receptors with (S)-1-[4-(dimethylamino)-3-methylphen
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