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1 other agents which are more specific for the alpha1 adrenergic receptor.
2 these modulatory effects are attributable to alpha1 adrenergic receptors.
3 mIPSCs frequency results from activation of alpha1 adrenergic receptors.
4 nformation describing this drug class at the alpha1-adrenergic receptors.
5 inity for dopamine D2, serotonin 5-HT1A, and alpha1-adrenergic receptors.
6 yl cyclase, and protein kinase A, as well as alpha1-adrenergic receptors.
7 E release and that this might be specific to alpha1-adrenergic receptors.
8 , thereby ruling out [3H]CUMI-101 binding to alpha1-adrenergic receptors.
9 PPG neurons, and this involved activation of alpha(1)-adrenergic receptors.
10 step in the agonist-dependent activation of alpha(1)-adrenergic receptors.
14 of cells with phenylephrine (PE), a specific alpha(1) adrenergic receptor agonist, increased protein
15 include insulin receptor substrate-1, as the alpha(1)-adrenergic receptor agonist also inhibited the
18 with phorbol 12-myristate 13-acetate or the alpha(1)-adrenergic receptor agonist norepinephrine via
19 of the cells with phenylephrine, a specific alpha(1)-adrenergic receptor agonist, activated p70 S6 k
21 Consistent with this idea, the selective alpha1-adrenergic receptor agonist methoxamine was still
22 cked the induction of these responses by the alpha1-adrenergic receptor agonist phenylephrine, wherea
23 ith either insulin or phenylephrine (PE), an alpha1-adrenergic receptor agonist, induced Ser-9 phosph
24 itoneally) or saline, the response to the a) alpha1-adrenergic receptor agonist, phenylephrine; b) en
25 was perturbed by intravenous injection of an alpha1-adrenergic receptor agonist, unilateral pressure
26 was perturbed by intravenous injection of an alpha1-adrenergic receptor agonist, unilateral pressure
28 sylated Rho and inhibited the characteristic alpha1-adrenergic receptor agonist-induced myofibrillar
31 are induced in cultured myocardial cells by alpha1- adrenergic receptor agonists, such as phenylephr
32 inately induced by growth promoters, such as alpha1-adrenergic receptor agonists (e.g. phenylephrine
39 through vasopressin receptor (V1A-R) but not alpha1 adrenergic receptor (alpha1-AR), suggesting that
40 rat ventricular myocytes, stimulation of the alpha1-adrenergic receptor (alpha1-AdrR) activates a pro
41 oth muscle, or to phenylephrine, a selective alpha1-adrenergic receptor (alpha1-AR) agonist, was simi
43 alpha1ABKO) mice that lacked cardiac myocyte alpha1-adrenergic receptor (alpha1-AR) binding, aortic c
44 ing mediated by the angiotensin (Ang) II and alpha1-adrenergic receptor (alpha1-AR) pathways is impor
50 loned cDNAs encoding three subtypes of human alpha1-adrenergic receptors (alpha1ARs), alpha1a, alpha1
53 ffects of NE are mediated through Gq-coupled alpha(1)-adrenergic receptors and are mimicked by the ac
54 ility was assessed by measuring affinity for alpha(1)-adrenergic receptors and inhibition of neuronal
55 is proposed as a coupling mechanism between alpha(1)-adrenergic receptors and phospholipase C (PLC),
56 botropic neurotransmitter receptors (mGluRs, alpha1 adrenergic receptors, and muscarinic acetylcholin
57 ease of dopamine, activation of postsynaptic alpha1 adrenergic receptors, and suppression of InsP3-in
58 constrictions in MA but not in MV while the alpha(1)-adrenergic receptor antagonist, prazosin (0.1 m
61 us losartan (10 mg/kg b.wt) nor prazosin, an alpha1 adrenergic receptor antagonist, at doses of 5 mic
63 e Cl- current to 5.9 nM, and addition of the alpha1-adrenergic receptor antagonist prazosin did not c
64 up of innervated pigs during pharmacological alpha(1)-adrenergic receptor (AR) blockade, infarct size
65 ling pathways linking activation of specific alpha(1)-adrenergic receptor (AR) subtypes to these phys
66 ular, we show that although both mGluR5- and alpha(1)-adrenergic receptor (AR)-dependent LTDs involve
68 61W retinal cells in high glucose and of the alpha1-adrenergic receptor (AR) on vascular lesions of t
71 hat the type 1 muscarinic receptor (m1R) and alpha1-adrenergic receptor (AR)-mediated SRF activation
77 studies have demonstrated that activation of alpha(1)-adrenergic receptors (ARs) increased interleuki
78 its role in the cardioprotective actions of alpha(1)-adrenergic receptors (ARs) remains uncertain, b
80 of blood pressure through interactions with alpha1-adrenergic receptors (ARs) in vascular smooth mus
81 direct evidence suggests that stimulation of alpha1-adrenergic receptors (ARs) increases smooth muscl
86 ral-midbrain dopaminergic neurons through an alpha1 adrenergic receptor-dependent mechanism within th
87 tes interfered with the basal expression and alpha1-adrenergic receptor-dependent activation of a TEF
91 he mechanism underlying the critical role of alpha1 adrenergic receptors in the regulation of dopamin
92 ed if insulin or IGF-I induced expression of alpha1 adrenergic receptors in vascular smooth muscle ce
93 hat significantly altered mRNA levels of the alpha1- adrenergic receptor in the basal forebrain as we
94 our recently demonstrated mechanism whereby alpha1-adrenergic receptors in the same cell type regula
96 oss bovine RPE by activating apical membrane alpha(1)-adrenergic receptors, increasing [Ca2+](in), an
102 70 gene expression induced by stimulation of alpha1 adrenergic receptors is markedly attenuated, whic
103 concurrent episodic activation of 5-HT2 and alpha1-adrenergic receptors is necessary to produce long
104 emonstrated lead evolution from heterocyclic alpha(1)-adrenergic receptor ligands to highly dissimila
109 ases neural stimulation of BAT and increases alpha1-adrenergic receptor number; however, the alpha1 r
111 that in MDCK-D1 cells, epinephrine acting on alpha1-adrenergic receptors, promotes a rapid increase i
112 In addition, we show that stimulation of alpha(1)-adrenergic receptor-protein kinase D1-Rem1 sign
113 ikewise, ANP and 8-bromo-cGMP attenuated the alpha1-adrenergic receptor- stimulated increase in prepr
114 imulated increase in prepro-ANP mRNA and the alpha1-adrenergic receptor-stimulated decrease in sarcop
115 re, in myocytes, 8-bromo-cGMP attenuated the alpha1-adrenergic receptor-stimulated increases in c-fos
121 the TGII mice at base line or in response to alpha(1)-adrenergic receptor stimulation; nor was protei
122 d signal transduction mechanisms involved in alpha1, adrenergic receptor stimulation of hsp7O gene ex
125 or (ANF) reporter gene expression induced by alpha1-adrenergic receptor stimulation with phenylephrin
126 neuronal progenitors colocalized with either alpha(1)-adrenergic receptor subtype in the olfactory bu
127 ing assays were used to examine the basis of alpha1-adrenergic receptor subtype selectivity for a ser
129 cent protein or constitutively active mutant alpha(1)-adrenergic receptor subtypes in tissues in whic
130 ated from normal mice expressed a mixture of alpha(1)-adrenergic receptor subtypes, and stimulation o
131 n significantly reduced gene expression of 3 alpha(1)-adrenergic receptor subtypes, consistent with b
132 with that previously described for the other alpha1 adrenergic receptor subtypes, may shed light on t
133 nsfected with each of the three cloned human alpha1 adrenergic receptor subtypes, norepinephrine stro
134 y episodic but not continuous stimulation of alpha1-adrenergic receptors that requires protein kinase
135 slated and active in costimulating, with the alpha1-adrenergic receptor, the firing of DR 5-HT neuron
137 was to determine the effect of endotoxin on alpha1-adrenergic receptor vasoconstriction and both end
138 tors, is also shown to be a modulator of the alpha1-adrenergic receptors, which suggests a general la
139 ncreases intracellular Ca(2+) similar to the alpha1 adrenergic receptor, while OAMB-K3 additionally s
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