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1 tuting individual transmembrane domains from alpha 1D adrenergic receptors.
2 PPG neurons, and this involved activation of alpha(1)-adrenergic receptors.
3  step in the agonist-dependent activation of alpha(1)-adrenergic receptors.
4              The binding affinities of 21 at alpha(1)-adrenergic receptors ([(3)H]prazosin, IC(50) =
5 ecipitates, thus directly demonstrating that alpha 1-adrenergic receptors activate the 85-kD cPLA2.
6 niform increase in cell dimension induced by alpha(1)-adrenergic receptor activation.
7 us expresses particularly high levels of the alpha(1D) adrenergic receptor (ADR) and we have previous
8 of cells with phenylephrine (PE), a specific alpha(1) adrenergic receptor agonist, increased protein
9 include insulin receptor substrate-1, as the alpha(1)-adrenergic receptor agonist also inhibited the
10                                The selective alpha(1)-adrenergic receptor agonist methoxamine had no
11                                          The alpha(1)-adrenergic receptor agonist norepinephrine sele
12  with phorbol 12-myristate 13-acetate or the alpha(1)-adrenergic receptor agonist norepinephrine via
13  of the cells with phenylephrine, a specific alpha(1)-adrenergic receptor agonist, activated p70 S6 k
14  in cardiomyocyte hypertrophy induced by the alpha 1-adrenergic receptor (alpha 1-AR) agonist phenyle
15                                          The alpha 1-adrenergic receptors (alpha 1-AR) belong to the
16                                Activation of alpha 1-adrenergic receptors (alpha 1-AR) increases Na+/
17                 In addition, Rlf potentiated alpha(1)-adrenergic receptor (alpha(1)-AR)-induced ANF e
18                           Catecholamines and alpha(1)-adrenergic receptors (alpha(1)-ARs) cause cardi
19 use of TCA drugs increases the expression of alpha(1)-adrenergic receptors (alpha(1)-ARs).
20                                  The role of alpha(1)-adrenergic receptors (alpha(1)ARs) in cognition
21                                              alpha(1)-adrenergic receptors (alpha(1)ARs) regulate blo
22                                              alpha(1)-Adrenergic receptors (alpha(1A), alpha(1B), and
23 y 11 and 12) that are the most selective for alpha(1d)-adrenergic receptors (alpha(1d)-AR) reported t
24                   Heterologous expression of alpha(1D)-adrenergic receptors (alpha(1D)-ARs) in most c
25                                              Alpha 1-adrenergic receptors (alpha1-ARs) control the ac
26                                              alpha(1)-Adrenergic receptors also activate a PKCdelta-P
27 ffects of NE are mediated through Gq-coupled alpha(1)-adrenergic receptors and are mimicked by the ac
28 ility was assessed by measuring affinity for alpha(1)-adrenergic receptors and inhibition of neuronal
29  is proposed as a coupling mechanism between alpha(1)-adrenergic receptors and phospholipase C (PLC),
30 ond experiment examined whether prazosin, an alpha 1-adrenergic receptor antagonist, could attenuate
31 nd this response was blocked by prazosin, an alpha 1-adrenergic receptor antagonist.
32  constrictions in MA but not in MV while the alpha(1)-adrenergic receptor antagonist, prazosin (0.1 m
33                        Pretreatment with the alpha(1)-adrenergic receptor antagonist, prazosin, and t
34                                 The specific alpha(1)-adrenergic receptor antagonist, prazosin, inhib
35  in patients with current or previous use of alpha-1 adrenergic receptor antagonists.
36                                              Alpha 1-adrenergic receptor (AR) activation is thought t
37 e compared the efficiencies with which human alpha 1-adrenergic receptor (AR) subtypes activate inosi
38                                              alpha 1-Adrenergic receptor (AR) subtypes mediate many e
39 up of innervated pigs during pharmacological alpha(1)-adrenergic receptor (AR) blockade, infarct size
40 ling pathways linking activation of specific alpha(1)-adrenergic receptor (AR) subtypes to these phys
41 ular, we show that although both mGluR5- and alpha(1)-adrenergic receptor (AR)-dependent LTDs involve
42 f sympathetic nervous system function is the alpha(1D)-adrenergic receptor (AR), which belongs to the
43                     The goal was to identify alpha-1-adrenergic receptor (AR) subtypes in human coron
44 ions have been found in vitro which maintain alpha 1-adrenergic receptors (ARs) in a partially activa
45                                              alpha 1-adrenergic receptors (ARs) play a major role in
46                                              alpha(1)-Adrenergic receptors (ARs) are not well defined
47                                              alpha(1)-Adrenergic receptors (ARs) belong to the large
48                                  The role of alpha(1)-adrenergic receptors (ARs) in the regulation of
49 studies have demonstrated that activation of alpha(1)-adrenergic receptors (ARs) increased interleuki
50  its role in the cardioprotective actions of alpha(1)-adrenergic receptors (ARs) remains uncertain, b
51                                              alpha(1D)-Adrenergic receptors (ARs) are key regulators
52     The epinephrine response was mediated by alpha 1 adrenergic receptors based on the greater potenc
53                    Our results indicate that alpha(1)-adrenergic receptors can regulate both neurogen
54 es, but the coupling of hhG alpha h with the alpha 1-adrenergic receptor did not increase.
55 ubtypes have been successfully cloned in the alpha 1-adrenergic receptor family, and they share 50% i
56    The existence of multiple subtypes of the alpha 1 adrenergic receptor has been demonstrated both p
57 e present study clearly demonstrate that the alpha 1-adrenergic receptor in human heart couples with
58         The understanding of the function of alpha(1)-adrenergic receptors in the brain has been limi
59 oss bovine RPE by activating apical membrane alpha(1)-adrenergic receptors, increasing [Ca2+](in), an
60                                Activation of alpha(1)-adrenergic receptors influences both the contra
61 anner, but the increase was abolished by the alpha(1D)-adrenergic receptor inhibitor BMY-7378.
62  human cardiac tissue, the expression of the alpha 1-adrenergic receptor is increased under pathophys
63                                   Potency at alpha(1) adrenergic receptors is low for the four cinnam
64          Agonist-dependent activation of the alpha(1)-adrenergic receptor is postulated to be initiat
65 emonstrated lead evolution from heterocyclic alpha(1)-adrenergic receptor ligands to highly dissimila
66                   In applying this method to alpha(1)-adrenergic receptor ligands, we have demonstrat
67                                              alpha(1) Adrenergic receptors mediate both vascular and
68 ed that the other components involved in the alpha 1-adrenergic receptor-mediated signaling pathway a
69                                          The alpha 1-adrenergic receptor mediates actions of the symp
70              In ischemic cardiomyopathy, the alpha 1-adrenergic receptor number increased twofold (27
71            PKC activity is implicated in the alpha(1)-adrenergic receptor pathway that activates PKD1
72 sm whereby a G protein-coupled receptor, the alpha 1-adrenergic receptor, promotes cellular AA releas
73     In addition, we show that stimulation of alpha(1)-adrenergic receptor-protein kinase D1-Rem1 sign
74  data thus demonstrate that in MDCK-D1 cells alpha 1-adrenergic receptors regulate AA release through
75 bited PLC activation induced by metabotropic alpha 1-adrenergic receptor signaling in cultured rat br
76  The effects of epinephrine were mediated by alpha 1-adrenergic receptors since they were blocked by
77                                      Neither alpha 1-adrenergic receptor stimulation with methoxamine
78                  Cardiac myocytes respond to alpha(1)-adrenergic receptor stimulation by a progressiv
79                                              alpha(1)-Adrenergic receptor stimulation increased the a
80       However, in adult normal neurospheres, alpha(1)-adrenergic receptor stimulation increased the e
81 ction caused by ischemic preconditioning and alpha(1)-adrenergic receptor stimulation.
82 the TGII mice at base line or in response to alpha(1)-adrenergic receptor stimulation; nor was protei
83 urther reports on the efficacy and safety of alpha 1-adrenergic receptor subtype selective agents hav
84 neuronal progenitors colocalized with either alpha(1)-adrenergic receptor subtype in the olfactory bu
85 cent protein or constitutively active mutant alpha(1)-adrenergic receptor subtypes in tissues in whic
86 ated from normal mice expressed a mixture of alpha(1)-adrenergic receptor subtypes, and stimulation o
87 n significantly reduced gene expression of 3 alpha(1)-adrenergic receptor subtypes, consistent with b
88 that Gh, which transfers the signal from the alpha 1-adrenergic receptor to the 69-kD phospholipase C

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