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1 other agents which are more specific for the alpha1 adrenergic receptor.
2 was improved by sub-chronically blocking the alpha1-adrenergic receptor.
3 these modulatory effects are attributable to alpha1 adrenergic receptors.
4  mIPSCs frequency results from activation of alpha1 adrenergic receptors.
5 inity for dopamine D2, serotonin 5-HT1A, and alpha1-adrenergic receptors.
6 , thereby ruling out [3H]CUMI-101 binding to alpha1-adrenergic receptors.
7 nformation describing this drug class at the alpha1-adrenergic receptors.
8 yl cyclase, and protein kinase A, as well as alpha1-adrenergic receptors.
9 E release and that this might be specific to alpha1-adrenergic receptors.
10 PPG neurons, and this involved activation of alpha(1)-adrenergic receptors.
11  step in the agonist-dependent activation of alpha(1)-adrenergic receptors.
12              The binding affinities of 21 at alpha(1)-adrenergic receptors ([(3)H]prazosin, IC(50) =
13               These results demonstrate that alpha1 adrenergic receptors activate the transcription f
14 niform increase in cell dimension induced by alpha(1)-adrenergic receptor activation.
15 onstrated impaired testicular vasomotion via alpha1-adrenergic receptor activation and increased hypo
16 of cells with phenylephrine (PE), a specific alpha(1) adrenergic receptor agonist, increased protein
17 include insulin receptor substrate-1, as the alpha(1)-adrenergic receptor agonist also inhibited the
18                                The selective alpha(1)-adrenergic receptor agonist methoxamine had no
19                                          The alpha(1)-adrenergic receptor agonist norepinephrine sele
20  with phorbol 12-myristate 13-acetate or the alpha(1)-adrenergic receptor agonist norepinephrine via
21  of the cells with phenylephrine, a specific alpha(1)-adrenergic receptor agonist, activated p70 S6 k
22 osolic free [Ca2+] oscillations evoked by an alpha1 adrenergic receptor agonist.
23     Consistent with this idea, the selective alpha1-adrenergic receptor agonist methoxamine was still
24 cked the induction of these responses by the alpha1-adrenergic receptor agonist phenylephrine, wherea
25 ith either insulin or phenylephrine (PE), an alpha1-adrenergic receptor agonist, induced Ser-9 phosph
26 itoneally) or saline, the response to the a) alpha1-adrenergic receptor agonist, phenylephrine; b) en
27 was perturbed by intravenous injection of an alpha1-adrenergic receptor agonist, unilateral pressure
28 was perturbed by intravenous injection of an alpha1-adrenergic receptor agonist, unilateral pressure
29 o phenylephrine (PE; 10(-10) to 10(-4)M), an alpha1-adrenergic receptor agonist, was examined.
30 sylated Rho and inhibited the characteristic alpha1-adrenergic receptor agonist-induced myofibrillar
31                                              alpha1-Adrenergic receptor agonist-induced myofibrilloge
32 rom the nucleus when cells were treated with alpha1-adrenergic receptor agonist.
33  are induced in cultured myocardial cells by alpha1- adrenergic receptor agonists, such as phenylephr
34 inately induced by growth promoters, such as alpha1-adrenergic receptor agonists (e.g. phenylephrine
35                 In addition, Rlf potentiated alpha(1)-adrenergic receptor (alpha(1)-AR)-induced ANF e
36     The locus coeruleus promotes arousal via alpha(1)-adrenergic receptor (alpha(1)AR)-driven recruit
37                           Catecholamines and alpha(1)-adrenergic receptors (alpha(1)-ARs) cause cardi
38                                              alpha(1)-adrenergic receptors (alpha(1)-ARs) play critic
39 use of TCA drugs increases the expression of alpha(1)-adrenergic receptors (alpha(1)-ARs).
40                                  The role of alpha(1)-adrenergic receptors (alpha(1)ARs) in cognition
41                                              alpha(1)-adrenergic receptors (alpha(1)ARs) regulate blo
42                                              alpha(1)-Adrenergic receptors (alpha(1A), alpha(1B), and
43 t in response to acute stress, activation of alpha(1)-adrenergic receptors (alpha1-Rs) on Purkinje ce
44  which were prevented by incubation with the alpha1 adrenergic receptor (alpha1-AR) antagonist prazos
45 through vasopressin receptor (V1A-R) but not alpha1 adrenergic receptor (alpha1-AR), suggesting that
46 rat ventricular myocytes, stimulation of the alpha1-adrenergic receptor (alpha1-AdrR) activates a pro
47 oth muscle, or to phenylephrine, a selective alpha1-adrenergic receptor (alpha1-AR) agonist, was simi
48                                           An alpha1-adrenergic receptor (alpha1-AR) antagonist increa
49 alpha1ABKO) mice that lacked cardiac myocyte alpha1-adrenergic receptor (alpha1-AR) binding, aortic c
50 ing mediated by the angiotensin (Ang) II and alpha1-adrenergic receptor (alpha1-AR) pathways is impor
51         This study determined the effects of alpha1-adrenergic receptor (alpha1-AR) stimulation by ph
52 elease in vascular smooth muscle coordinates alpha1-adrenergic receptor (alpha1-AR) vasoconstriction
53                                              alpha1-Adrenergic receptor (alpha1-ARs) subtypes (alpha1
54 serotonin dorsal raphe neurons is driven via alpha1-adrenergic receptors (alpha1-A(R)) activation.
55 n, noradrenaline activates G-protein-coupled alpha1-adrenergic receptors (alpha1-A(R)) causing action
56 n, noradrenaline activates Galpha(q)-coupled alpha1-adrenergic receptors (alpha1-A(R)), causing actio
57 tion potentials via activation of excitatory alpha1-adrenergic receptors (alpha1-A(R)).
58                                              alpha1-Adrenergic receptors (alpha1-ARs) are members of
59 4(SMC) channels to the constrictor effect of alpha1 adrenergic receptor (alpha1AR) stimulation and el
60        A growing body of evidence implicates alpha1-adrenergic receptors (alpha1ARs) as potent regula
61       Similarly, agonist stimulation of vPAG alpha1-adrenergic receptors (alpha1ARs) increased latenc
62                                          The alpha1-adrenergic receptors (alpha1ARs) play an importan
63 loned cDNAs encoding three subtypes of human alpha1-adrenergic receptors (alpha1ARs), alpha1a, alpha1
64 litating dopamine (DA) neurotransmission via alpha1-adrenergic receptors (alpha1ARs).
65                                              alpha(1)-Adrenergic receptors also activate a PKCdelta-P
66 hout lowering heart rate by dual blockade of alpha(1)-adrenergic receptor and RyR2 in mouse and human
67 ffects of NE are mediated through Gq-coupled alpha(1)-adrenergic receptors and are mimicked by the ac
68 ility was assessed by measuring affinity for alpha(1)-adrenergic receptors and inhibition of neuronal
69  is proposed as a coupling mechanism between alpha(1)-adrenergic receptors and phospholipase C (PLC),
70 botropic neurotransmitter receptors (mGluRs, alpha1 adrenergic receptors, and muscarinic acetylcholin
71 ease of dopamine, activation of postsynaptic alpha1 adrenergic receptors, and suppression of InsP3-in
72  constrictions in MA but not in MV while the alpha(1)-adrenergic receptor antagonist, prazosin (0.1 m
73                        Pretreatment with the alpha(1)-adrenergic receptor antagonist, prazosin, and t
74                                 The specific alpha(1)-adrenergic receptor antagonist, prazosin, inhib
75 us losartan (10 mg/kg b.wt) nor prazosin, an alpha1 adrenergic receptor antagonist, at doses of 5 mic
76                                          The alpha1-adrenergic receptor antagonist prazosin (0.1 micr
77 e Cl- current to 5.9 nM, and addition of the alpha1-adrenergic receptor antagonist prazosin did not c
78 drenergic receptor antagonist) and prazosin (alpha1-adrenergic receptor antagonist) reduced female bu
79 up of innervated pigs during pharmacological alpha(1)-adrenergic receptor (AR) blockade, infarct size
80 ling pathways linking activation of specific alpha(1)-adrenergic receptor (AR) subtypes to these phys
81 ular, we show that although both mGluR5- and alpha(1)-adrenergic receptor (AR)-dependent LTDs involve
82                 Activation of the endogenous alpha1-adrenergic receptor (AR) associated with human ao
83 heteromerize with one or more members of the alpha1-adrenergic receptor (AR) family in recombinant sy
84 61W retinal cells in high glucose and of the alpha1-adrenergic receptor (AR) on vascular lesions of t
85                                              alpha1-Adrenergic receptor (AR) subtypes in the heart ar
86                             The three cloned alpha1-adrenergic receptor (AR) subtypes, alpha1B, alpha
87 hat the type 1 muscarinic receptor (m1R) and alpha1-adrenergic receptor (AR)-mediated SRF activation
88                                              alpha1 adrenergic receptors are known to activate protei
89                                          The alpha1-adrenergic receptors are targets for a number of
90                                              alpha(1)-Adrenergic receptors (ARs) are not well defined
91                                              alpha(1)-Adrenergic receptors (ARs) belong to the large
92                                  The role of alpha(1)-adrenergic receptors (ARs) in the regulation of
93 studies have demonstrated that activation of alpha(1)-adrenergic receptors (ARs) increased interleuki
94  its role in the cardioprotective actions of alpha(1)-adrenergic receptors (ARs) remains uncertain, b
95 V)1.2 as a principal target for G(q)-coupled alpha(1)-adrenergic receptors (ARs).
96                                              alpha1-Adrenergic receptors (ARs) are well-known mediato
97  of blood pressure through interactions with alpha1-adrenergic receptors (ARs) in vascular smooth mus
98 direct evidence suggests that stimulation of alpha1-adrenergic receptors (ARs) increases smooth muscl
99 ith POTS (98.3%) and all controls (100%) had alpha1 adrenergic receptor autoantibody concentrations a
100  inhibited by OAG exposure or stimulation of alpha1-adrenergic receptors by phenylephrine.
101                    Our results indicate that alpha(1)-adrenergic receptors can regulate both neurogen
102                               We wondered if alpha1 adrenergic receptors could activate transcription
103 we show that in vivo respiratory LTF is also alpha1-adrenergic receptor dependent.
104 ral-midbrain dopaminergic neurons through an alpha1 adrenergic receptor-dependent mechanism within th
105 tes interfered with the basal expression and alpha1-adrenergic receptor-dependent activation of a TEF
106 ric nuclear-retained Vgl-4 protein inhibited alpha1-adrenergic receptor-dependent activation.
107                  We previously reported that alpha(1)-adrenergic receptors drive moderate alcohol int
108  angiotensin II (Ang II) type 1 receptor and alpha1-adrenergic receptors has been described.
109         The understanding of the function of alpha(1)-adrenergic receptors in the brain has been limi
110 he mechanism underlying the critical role of alpha1 adrenergic receptors in the regulation of dopamin
111 ed if insulin or IGF-I induced expression of alpha1 adrenergic receptors in vascular smooth muscle ce
112 hat significantly altered mRNA levels of the alpha1- adrenergic receptor in the basal forebrain as we
113  our recently demonstrated mechanism whereby alpha1-adrenergic receptors in the same cell type regula
114                                Activation of alpha1 adrenergic receptors increased cAMP accumulation
115 oss bovine RPE by activating apical membrane alpha(1)-adrenergic receptors, increasing [Ca2+](in), an
116                                 In addition, alpha1 adrenergic receptor-induced CREB phosphorylation
117                                Activation of alpha(1)-adrenergic receptors influences both the contra
118 uctive tract, it has been suggested that the alpha1-adrenergic receptor influences fertility and sper
119 ion, while maintaining stroke volume through alpha(1)-adrenergic receptor inhibition in vivo.
120              Control patients not taking any alpha1 adrenergic receptor inhibtors were also dilated w
121                                   Potency at alpha(1) adrenergic receptors is low for the four cinnam
122          Agonist-dependent activation of the alpha(1)-adrenergic receptor is postulated to be initiat
123 70 gene expression induced by stimulation of alpha1 adrenergic receptors is markedly attenuated, whic
124  concurrent episodic activation of 5-HT2 and alpha1-adrenergic receptors is necessary to produce long
125 emonstrated lead evolution from heterocyclic alpha(1)-adrenergic receptor ligands to highly dissimila
126                   In applying this method to alpha(1)-adrenergic receptor ligands, we have demonstrat
127                                              alpha(1) Adrenergic receptors mediate both vascular and
128  examine the possible requirement for Rho in alpha1-adrenergic receptor-mediated hypertrophy.
129                                Activation of alpha1 adrenergic receptors not only stimulates smooth m
130 ases neural stimulation of BAT and increases alpha1-adrenergic receptor number; however, the alpha1 r
131 t of hypertension and inhibition of systemic alpha1-adrenergic receptor or angiotensin II AT1 recepto
132            PKC activity is implicated in the alpha(1)-adrenergic receptor pathway that activates PKD1
133 that in MDCK-D1 cells, epinephrine acting on alpha1-adrenergic receptors, promotes a rapid increase i
134     In addition, we show that stimulation of alpha(1)-adrenergic receptor-protein kinase D1-Rem1 sign
135 ikewise, ANP and 8-bromo-cGMP attenuated the alpha1-adrenergic receptor- stimulated increase in prepr
136 imulated increase in prepro-ANP mRNA and the alpha1-adrenergic receptor-stimulated decrease in sarcop
137 re, in myocytes, 8-bromo-cGMP attenuated the alpha1-adrenergic receptor-stimulated increases in c-fos
138                                Activation of alpha1 adrenergic receptors stimulates mitogenesis in hu
139                  Cardiac myocytes respond to alpha(1)-adrenergic receptor stimulation by a progressiv
140                                              alpha(1)-Adrenergic receptor stimulation increased the a
141       However, in adult normal neurospheres, alpha(1)-adrenergic receptor stimulation increased the e
142 ction caused by ischemic preconditioning and alpha(1)-adrenergic receptor stimulation.
143 the TGII mice at base line or in response to alpha(1)-adrenergic receptor stimulation; nor was protei
144 d signal transduction mechanisms involved in alpha1, adrenergic receptor stimulation of hsp7O gene ex
145                                              alpha1-Adrenergic receptor stimulation can inhibit the C
146                                              Alpha1-adrenergic receptor stimulation induces cardiac m
147 or (ANF) reporter gene expression induced by alpha1-adrenergic receptor stimulation with phenylephrin
148 neuronal progenitors colocalized with either alpha(1)-adrenergic receptor subtype in the olfactory bu
149 ing assays were used to examine the basis of alpha1-adrenergic receptor subtype selectivity for a ser
150              Epinephrine, acting through the alpha1-adrenergic receptor subtype, promoted transient t
151 cent protein or constitutively active mutant alpha(1)-adrenergic receptor subtypes in tissues in whic
152 ated from normal mice expressed a mixture of alpha(1)-adrenergic receptor subtypes, and stimulation o
153 n significantly reduced gene expression of 3 alpha(1)-adrenergic receptor subtypes, consistent with b
154 with that previously described for the other alpha1 adrenergic receptor subtypes, may shed light on t
155 nsfected with each of the three cloned human alpha1 adrenergic receptor subtypes, norepinephrine stro
156 erebellar cortex or BG-specific knockdown of alpha(1)-adrenergic receptors suppressed BG flares, redu
157 y episodic but not continuous stimulation of alpha1-adrenergic receptors that requires protein kinase
158 slated and active in costimulating, with the alpha1-adrenergic receptor, the firing of DR 5-HT neuron
159                      Noradrenaline activated alpha1-adrenergic receptors to increase GABA(A)-IPSC fre
160                          Activation of glial alpha1-adrenergic receptors triggers rapid astrocytic Ca
161  was to determine the effect of endotoxin on alpha1-adrenergic receptor vasoconstriction and both end
162 tors, is also shown to be a modulator of the alpha1-adrenergic receptors, which suggests a general la
163 ncreases intracellular Ca(2+) similar to the alpha1 adrenergic receptor, while OAMB-K3 additionally s

 
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