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1 PNMT inhibitory potency and affinity for the alpha2-adrenoceptor.
2 s inhibitors of PNMT and for affinity at the alpha2-adrenoceptor.
3 nd to be antagonists/inverse agonists of the alpha2-adrenoceptor.
4 mpounds also exhibit strong affinity for the alpha2-adrenoceptor.
5 is reduction is evident for both alpha1- and alpha2-adrenoceptors.
6 ne, consistent with an action at presynaptic alpha2-adrenoceptors.
7 urnover, by negative feedback regulation via alpha2-adrenoceptors.
8  with conflicting functional activity at the alpha2-adrenoceptor, a G-protein-coupled receptor with r
9 ly isolated LC neurons to examine opioid and alpha2-adrenoceptor action on potassium and calcium curr
10                                     In fact, alpha2-adrenoceptor activation, which is known to stimul
11 responsible for PNMT inhibitory activity and alpha2-adrenoceptor affinity were investigated by evalua
12               To design a selective (PNMT vs alpha2-adrenoceptor affinity) inhibitor of PNMT, the ste
13  the design of potent and selective (PNMT vs alpha2-adrenoceptor affinity) inhibitors of PNMT.
14 ase (PNMT, EC 2.1.1.28), with respect to its alpha2-adrenoceptor affinity, than is 3-methyl-1,2,3, 4-
15 d in the PNMT active site and possess little alpha2-adrenoceptor affinity, thereby conferring good se
16        In infant rats, administration of the alpha2 adrenoceptor agonist clonidine simultaneously evo
17  (10 micro M), and occluded partially by the alpha2 adrenoceptor agonist UK14,304 (10 micro M) as wel
18 low-dose dexmedetomidine, a highly selective alpha2 adrenoceptor agonist, could safely decrease the i
19 ee of EPSC depression was also seen with the alpha2-adrenoceptor agonist clonidine (5 microM), and th
20   We showed previously that injection of the alpha2-adrenoceptor agonist clonidine at the site of per
21 mplitude of potassium current induced by the alpha2-adrenoceptor agonist UK14304 was not significantl
22 .573) and a three-parameter equation for the alpha2-adrenoceptor (alpha2 pKi = 0.599pi - 0.0542MR - 0
23           These effects were mimicked by the alpha2-adrenoceptor (alpha2-AR) agonist guanabenz, but n
24 ontal cortex through actions at postsynaptic alpha2-adrenoceptors (alpha2-AR).
25 y increased constrictor activity of vascular alpha2-adrenoceptors (alpha2-ARs).
26 rough the actions of noradrenaline at spinal alpha2 -adrenoceptors, although serotonin, acting on fac
27 s or i.c.v. pretreatment with yohimbine, the alpha2-adrenoceptor and 5-HT1A receptor antagonist, bloc
28 e similar at the PNMT active site and at the alpha2-adrenoceptor and that the electrostatic interacti
29 decreases in MAP and HR possibly via central alpha2-adrenoceptor and/or 5-HT1A receptors and not thro
30 mediate inhibition of transmitter release by alpha2-adrenoceptors and represent important regulators
31 e LC was studied because elevated amounts of alpha2-adrenoceptors and tyrosine hydroxylase have been
32 ttenuated partially by pretreatment with the alpha2 adrenoceptor antagonist yohimbine (10 micro M), a
33                                          The alpha2 adrenoceptor antagonist yohimbine (YO) increases
34 ated in rats pretreated with atipamezole, an alpha2 adrenoceptor antagonist.
35             Pretreatment with yohimbine, the alpha2-adrenoceptor antagonist (8 microg; 5 microl; i.c.
36 blocked by intrathecal administration of the alpha2-adrenoceptor antagonist idazoxan and intra-LC co-
37                                          The alpha2-adrenoceptor antagonist yohimbine (YOH) was injec
38 ipants were administered hydrocortisone, the alpha2-adrenoceptor antagonist yohimbine, or both before
39 e shown that local infusions of NE or of the alpha2-adrenoceptor antagonist, atipamezole, in the mous
40  suggested that (11)C-yohimbine, a selective alpha2-adrenoceptor antagonist, is an appropriate ligand
41 t can be reduced by intrathecal injection of alpha2-adrenoceptor antagonists.
42                           More specifically, alpha2-adrenoceptors appear to mediate the antinocicepti
43 lerance at both the PNMT active site and the alpha2-adrenoceptor appears to be the same.
44                                              alpha2-Adrenoceptor (AR) agonists increase in analgesic
45 female rats with estrogen for 2 days reduces alpha2-adrenoceptor binding density by 25%, increases G
46 HE, enhanced norepinephrine release, whereas alpha2-adrenoceptor blockade attenuated it.
47                                    Selective alpha2-adrenoceptor blockade with yohimbine (0.6-1.0 mg/
48 re, the compounds exert their effects at the alpha2-adrenoceptor both in vitro in human prefrontal co
49 s and is quite selective for PNMT versus the alpha2-adrenoceptor, but 24 is less potent than the corr
50                                  In the PVN, alpha2-adrenoceptors do not appear to contribute to thes
51 e results suggest that estrogen may decrease alpha2-adrenoceptor expression in the frontal cortex of
52       The maps of (11)C-yohimbine binding to alpha2 adrenoceptors in human brain had the highest valu
53 ss of the tracer (11)C-yohimbine for mapping alpha2 adrenoceptors in human brain in vivo.
54 on-specific change in the sensitivity of the alpha2-adrenoceptor in isolates.
55 ; and enhanced expression and sensitivity of alpha2-adrenoceptors in the LC.
56 l periaqueductal gray is mediated in part by alpha2-adrenoceptors in the spinal cord dorsal horn.
57 le mutant in cells treated with PTX restored alpha2-adrenoceptor inhibition.
58 nd Galphai as mediators of the PTX-sensitive alpha2-adrenoceptor-mediated inhibition of N-type Ca2+ c
59 ayed by endogenous G-protein subunits in the alpha2-adrenoceptor-mediated inhibition of N-type Ca2+ c
60 d behavioral actions mediated by alpha1- and alpha2-adrenoceptors on neurons in the nucleus raphe mag
61 sser extent the glycine site) or stimulating alpha2-adrenoceptors, profoundly increases AADC activity
62 est the efficacy and mechanisms of action of alpha2-adrenoceptor stimulation to reduce pain.
63                   These results suggest that alpha2-adrenoceptor stimulation transforms cytokine gene
64 he production of nitric oxide in response to alpha2-adrenoceptor stimulation.
65 ir sedative/hypnotic properties although the alpha2 adrenoceptor subtype responsible for these anesth
66   In conclusion, NE inhibits LSI neurons via alpha2-adrenoceptor subtypes.
67  region, suggesting the involvement of other alpha2-adrenoceptor subtypes.
68 agonist, is an appropriate ligand for PET of alpha2 adrenoceptors that passes readily from blood to b
69  at the PNMT active site more so than at the alpha2-adrenoceptor (thus reducing selectivity).
70 ty and 2) the coupling of both mu-opioid and alpha2-adrenoceptors to calcium channels seems to be mor
71                    The results indicate that alpha2-adrenoceptors tonically restrain NE synthesis, re
72                 These findings indicate that alpha2-adrenoceptors trigger signals that protect the in
73 increased activity of vascular smooth muscle alpha2-adrenoceptors (VSM alpha2-ARs).
74 he specificity of (11)C-ORM-13070 binding to alpha2 adrenoceptors was demonstrated in rats pretreated
75 nucleus and reducing the affinity toward the alpha2-adrenoceptor was observed with this 3, 7-disubsti
76  antidepressant-free suicides, the number of alpha2-adrenoceptors was significantly higher in tempora
77 THIQ reduced the binding affinity toward the alpha2-adrenoceptor, we investigated the combination of
78 ted suicides, significantly lower numbers of alpha2-adrenoceptors were found in occipital cortex and
79                     alpha1-Adrenoceptors and alpha2-adrenoceptors were measured by radioligand bindin
80 phrine transporter, monoamine oxidase A, and alpha2-adrenoceptors were measured.
81  immunoreactivity and radioligand binding to alpha2-adrenoceptors were significantly lower (approxima

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