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1 his effect is most probably mediated through alpha-adrenergic receptors.
2 ses in FVC that are exclusively mediated via alpha-adrenergic receptors.
3 ganglion neurons evidencing the presence of alpha-adrenergic receptors.
4 ed by its intrinsic ability to also activate alpha-adrenergic receptors.
5 ined for 4 days in culture, we now show that alpha-adrenergic receptor activation by phenylephrine ca
6 salgia and for increased expression of human alpha-adrenergic receptors after loss of sympathetic act
8 ipocytes were treated with phenylephrine, an alpha-adrenergic receptor agonist, to drive HDACS out of
9 rpose of this study was to determine whether alpha-adrenergic receptor agonists have a role in alveol
13 tension, we investigated the role of central alpha-adrenergic receptors and CRF in mediating differen
15 netic variants of beta-adrenergic receptors, alpha-adrenergic receptors, and endothelin receptors (am
17 189254 effect was completely reversed by the alpha-adrenergic receptor antagonist phentolamine (i.p.
18 C) for 4 h or by intravenous infusion of the alpha-adrenergic receptor antagonist phentolamine for on
19 from the SPGN terminal, because neither the alpha-adrenergic receptor antagonist phentolamine nor th
21 textual fear conditioning, injections of the alpha-adrenergic receptor antagonist prazosin (1.0 or 3.
22 ed with saline, phentolamine, a nonselective alpha-adrenergic receptor antagonist, or propranolol, a
24 ostatic hyperplasia is commonly treated with alpha-adrenergic-receptor antagonists (alpha-blockers) o
25 inhibited phospholipase C activation by the alpha-adrenergic receptor (AR) agonist phenylephrine, su
26 f the present study was to determine whether alpha-adrenergic receptor (AR) constriction of venular s
27 hetic nervous system mediated principally by alpha-adrenergic receptors because phentolamine, but not
29 of studies aimed at examining the effects of alpha-adrenergic receptor blockade on LH secretion and t
31 erazinylthiocarbonyl) disulfide (FLA-63), or alpha-adrenergic receptor blockade with phenoxybenzamine
33 ing forearm evoke vasodilatation after local alpha-adrenergic receptor blockade, raising the possibil
35 and benign prostatic hyperplasia with either alpha adrenergic receptor blockers or 5alpha-reductase i
37 studies, we considered two receptors in the alpha-adrenergic receptor family, alpha2A and alpha2C, a
39 These results confirm the involvement of the alpha-adrenergic receptor in extinction processes in bot
41 the hypothesis that increased expression of alpha-adrenergic receptors in primary afferent neurons i
42 ypothesis proposes the increased presence of alpha-adrenergic receptors in primary afferent neurons t
43 nt, demonstrating a novel mechanism by which alpha-adrenergic receptors may regulate ion channel acti
44 ductance (FVC) and the contribution of local alpha-adrenergic receptor-mediated pathways to the obser
45 o suppression of mutant channel bursting via alpha-adrenergic receptor-mediated stimulation of PKC.
46 earm vascular conductance (FVC) responses to alpha-adrenergic receptor stimulation during rhythmic ha
47 rm vascular conductance (FVC) in response to alpha-adrenergic receptor stimulation during rhythmic ha
54 ubstitution on ligand binding and agonism of alpha-adrenergic receptor subtypes alpha1a, alpha1b, alp
56 Our results demonstrate that post-junctional alpha-adrenergic receptor vasoconstrictor responsiveness
58 of the mu-opioid receptor (MOR), but not of alpha-adrenergic receptors, which activate the same pool
59 current study examined whether antagonism of alpha-adrenergic receptors would impair the consolidatio
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