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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.
5 ecipitates, thus directly demonstrating that alpha 1-adrenergic receptors activate the 85-kD cPLA2.
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
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
23 y 11 and 12) that are the most selective for alpha(1d)-adrenergic receptors (alpha(1d)-AR) reported t
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
32 constrictions in MA but not in MV while the alpha(1)-adrenergic receptor antagonist, prazosin (0.1 m
37 e compared the efficiencies with which human alpha 1-adrenergic receptor (AR) subtypes activate inosi
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
44 ions have been found in vitro which maintain alpha 1-adrenergic receptors (ARs) in a partially activa
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
52 The epinephrine response was mediated by alpha 1 adrenergic receptors based on the greater potenc
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
59 oss bovine RPE by activating apical membrane alpha(1)-adrenergic receptors, increasing [Ca2+](in), an
62 human cardiac tissue, the expression of the alpha 1-adrenergic receptor is increased under pathophys
65 emonstrated lead evolution from heterocyclic alpha(1)-adrenergic receptor ligands to highly dissimila
68 ed that the other components involved in the alpha 1-adrenergic receptor-mediated signaling pathway a
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
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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