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1 mpounds also exhibit strong affinity for the alpha2-adrenoceptor.
2 PNMT inhibitory potency and affinity for the alpha2-adrenoceptor.
3 nd to be antagonists/inverse agonists of the alpha2-adrenoceptor.
4 s inhibitors of PNMT and for affinity at the alpha2-adrenoceptor.
5 urnover, by negative feedback regulation via alpha2-adrenoceptors.
6 is reduction is evident for both alpha1- and alpha2-adrenoceptors.
7 ne, consistent with an action at presynaptic alpha2-adrenoceptors.
8 en prepared and evaluated as ligands for the alpha(2) adrenoceptor.
9 isplay the opposite stereoselectivity at the alpha(2)-adrenoceptor.
10 d and evaluated for affinity at PNMT and the alpha(2)-adrenoceptor.
11 nhibitors of the binding of clonidine at the alpha(2)-adrenoceptor.
12 ) results in a reduction in affinity for the alpha(2)-adrenoceptor.
13 elective due to significant affinity for the alpha(2)-adrenoceptor.
14 highly selective due to low affinity for the alpha(2)-adrenoceptor.
15 NMT) inhibitory potency and affinity for the alpha(2)-adrenoceptor.
16 itors of PNMT and for their affinity for the alpha(2)-adrenoceptor.
17 sion via mechanisms that are specific to the alpha(2)-adrenoceptor.
18 nhibitors of the binding of clonidine at the alpha(2)-adrenoceptor.
19 was mediated by N-methyl-D-aspartate and/or alpha(2)-adrenoceptors.
20 idazoline sites but rather the activation of alpha(2)-adrenoceptors.
21 hanism of action of the drug is to stimulate alpha(2)-adrenoceptors.
22 action which likely involves stimulation of alpha(2)-adrenoceptors.
23 with conflicting functional activity at the alpha2-adrenoceptor, a G-protein-coupled receptor with r
24 ly isolated LC neurons to examine opioid and alpha2-adrenoceptor action on potassium and calcium curr
25 esent study investigated the hypothesis that alpha(2)-adrenoceptor activation inhibits icilin-induced
29 lethanolamine N-methyltransferase (PNMT) and alpha(2)-adrenoceptor affinities were predicted through
30 uent was found to have a major effect on the alpha(2)-adrenoceptor affinity of these compounds with t
31 drenoceptor, while the latter were devoid of alpha(2)-adrenoceptor affinity, but also lost potency at
32 responsible for PNMT inhibitory activity and alpha2-adrenoceptor affinity were investigated by evalua
35 ase (PNMT, EC 2.1.1.28), with respect to its alpha2-adrenoceptor affinity, than is 3-methyl-1,2,3, 4-
36 d in the PNMT active site and possess little alpha2-adrenoceptor affinity, thereby conferring good se
38 anol abolishes the hypotensive effect of the alpha(2)-adrenoceptor agonist clonidine in this rat mode
39 noamine oxidase (MAO) inhibitor harmane, the alpha(2)-adrenoceptor agonist clonidine, the mu-opioid r
40 tudy, we examined the effect of brimonidine (alpha(2)-adrenoceptor agonist) on RGC survival after inc
42 fects of dexmedetomidine, a highly selective alpha(2)-adrenoceptor agonist, on extracellular dopamine
43 Pretreatment with a peripherally restricted alpha(2)-adrenoceptor agonist, ST91 (0.075, 0.15 mg/kg),
45 (10 micro M), and occluded partially by the alpha2 adrenoceptor agonist UK14,304 (10 micro M) as wel
46 low-dose dexmedetomidine, a highly selective alpha2 adrenoceptor agonist, could safely decrease the i
47 ee of EPSC depression was also seen with the alpha2-adrenoceptor agonist clonidine (5 microM), and th
48 We showed previously that injection of the alpha2-adrenoceptor agonist clonidine at the site of per
49 mplitude of potassium current induced by the alpha2-adrenoceptor agonist UK14304 was not significantl
50 e demonstrated that the analgesic actions of alpha(2) adrenoceptor agonists are mediated by the alpha
52 the notion that the protective action of the alpha(2)-adrenoceptor agonists does not involve imidazol
53 In addition, the neuroprotective effect of alpha(2)-adrenoceptor agonists in the retina may involve
56 dy is that the neuroprotective properties of alpha(2)-adrenoceptor agonists, like clonidine, are very
61 .573) and a three-parameter equation for the alpha2-adrenoceptor (alpha2 pKi = 0.599pi - 0.0542MR - 0
65 rough the actions of noradrenaline at spinal alpha2 -adrenoceptors, although serotonin, acting on fac
66 methyl-THIQs are too potent (too hot) at the alpha(2)-adrenoceptor and the 3-trifluoromethyl-THIQs ar
67 1,2,3,4-tetrahydroisoquinoline (THIQ) at the alpha(2)-adrenoceptor and to the decreased pK(a) of the
68 zed Wistar rats, we have studied the role of alpha(2)-adrenoceptors and neuropeptide Y (NPY) Y(1) rec
69 s or i.c.v. pretreatment with yohimbine, the alpha2-adrenoceptor and 5-HT1A receptor antagonist, bloc
70 e similar at the PNMT active site and at the alpha2-adrenoceptor and that the electrostatic interacti
71 decreases in MAP and HR possibly via central alpha2-adrenoceptor and/or 5-HT1A receptors and not thro
72 mediate inhibition of transmitter release by alpha2-adrenoceptors and represent important regulators
73 e LC was studied because elevated amounts of alpha2-adrenoceptors and tyrosine hydroxylase have been
74 The alpha(1) adrenoceptor antagonist WB4101, alpha(2) adrenoceptor antagonist yohimbine and mu-opioid
76 idence of local noradrenaline release as the alpha(2)-adrenoceptor antagonist yohimbine increased the
77 ly reversed antinociception, but neither the alpha(2)-adrenoceptor antagonist yohimbine nor the alpha
79 a(1)-adrenoceptor antagonist), yohimbine (an alpha(2)-adrenoceptor antagonist) and phentolamine (a no
81 nt and co-infusion with the highly selective alpha(2)-adrenoceptor antagonist, atipamezole (ATZ).
82 ttenuated partially by pretreatment with the alpha2 adrenoceptor antagonist yohimbine (10 micro M), a
86 blocked by intrathecal administration of the alpha2-adrenoceptor antagonist idazoxan and intra-LC co-
88 ipants were administered hydrocortisone, the alpha2-adrenoceptor antagonist yohimbine, or both before
89 e shown that local infusions of NE or of the alpha2-adrenoceptor antagonist, atipamezole, in the mous
90 suggested that (11)C-yohimbine, a selective alpha2-adrenoceptor antagonist, is an appropriate ligand
91 effect of clonidine was attenuated when the alpha(2)-adrenoceptor antagonists yohimbine or rauwolsci
96 female rats with estrogen for 2 days reduces alpha2-adrenoceptor binding density by 25%, increases G
99 re, the compounds exert their effects at the alpha2-adrenoceptor both in vitro in human prefrontal co
100 s and is quite selective for PNMT versus the alpha2-adrenoceptor, but 24 is less potent than the corr
102 dicate that vasoconstricting post-junctional alpha(2)-adrenoceptors contribute more to basal vascular
104 e results suggest that estrogen may decrease alpha2-adrenoceptor expression in the frontal cortex of
105 more potent enantiomer at both PNMT and the alpha(2)-adrenoceptor for these 3-fluoromethyl-, 3-hydro
106 epinephrine mediates the analgesic action at alpha(2) adrenoceptors in the spinal cord, we now invest
107 e findings do not favor a role for brainstem alpha(2)-adrenoceptors in ethanol-induced attenuation of
108 the density (B(max)) and affinity (K(D)) of alpha(2)-adrenoceptors in the middle (mNTS) and rostral
109 r inhibits nociception through the action of alpha(2)-adrenoceptors in the spinal cord dorsal horn.
114 l periaqueductal gray is mediated in part by alpha2-adrenoceptors in the spinal cord dorsal horn.
115 mers of these compounds at both PNMT and the alpha(2)-adrenoceptor indicates that both sites display
117 greater than 0.57 and display selectivities (alpha(2)-adrenoceptor K(i)/PNMT K(i)) greater than 200 a
118 ors in this study and display selectivities (alpha(2)-adrenoceptor K(i)/PNMT K(i)) greater than 200.
120 ata we propose that exogenous and endogenous alpha(2) adrenoceptor ligands activate different alpha(2
122 onstrated that post-junctional alpha(1)- and alpha(2)-adrenoceptors mediate vasoconstriction in the h
123 These data provide the first evidence for alpha(2)-adrenoceptor-mediated constriction in slow-twit
124 nd Galphai as mediators of the PTX-sensitive alpha2-adrenoceptor-mediated inhibition of N-type Ca2+ c
125 ayed by endogenous G-protein subunits in the alpha2-adrenoceptor-mediated inhibition of N-type Ca2+ c
127 d behavioral actions mediated by alpha1- and alpha2-adrenoceptors on neurons in the nucleus raphe mag
128 sser extent the glycine site) or stimulating alpha2-adrenoceptors, profoundly increases AADC activity
129 P accumulation by modifying alpha(1)- and/or alpha(2)-adrenoceptor rather than beta-adrenoceptor sign
130 14,304 to selectively activate alpha(1)- or alpha(2)-adrenoceptors resulted in concentration-depende
132 increases in peripheral, as well as central, alpha(2)-adrenoceptor signaling oppose the behavioral st
137 ponsible for this analgesic action and which alpha(2) adrenoceptor subtype mediates this property.
138 ir sedative/hypnotic properties although the alpha2 adrenoceptor subtype responsible for these anesth
140 a(2) adrenoceptor ligands activate different alpha(2) adrenoceptor subtypes to produce their analgesi
143 agonist, is an appropriate ligand for PET of alpha2 adrenoceptors that passes readily from blood to b
145 ty and 2) the coupling of both mu-opioid and alpha2-adrenoceptors to calcium channels seems to be mor
149 he specificity of (11)C-ORM-13070 binding to alpha2 adrenoceptors was demonstrated in rats pretreated
150 nucleus and reducing the affinity toward the alpha2-adrenoceptor was observed with this 3, 7-disubsti
151 antidepressant-free suicides, the number of alpha2-adrenoceptors was significantly higher in tempora
152 THIQ reduced the binding affinity toward the alpha2-adrenoceptor, we investigated the combination of
153 ted suicides, significantly lower numbers of alpha2-adrenoceptors were found in occipital cortex and
156 immunoreactivity and radioligand binding to alpha2-adrenoceptors were significantly lower (approxima
157 reochemical preferences of both PNMT and the alpha(2)-adrenoceptor, which should assist in the develo
158 PNMT due to their decreased affinity for the alpha(2)-adrenoceptor, which was attributed to steric bu
160 n Ca(V)2.2 inhibition by norepinephrine (via alpha(2)-adrenoceptors, which do not bind NHERF2), nor o
161 elective due to significant affinity for the alpha(2)-adrenoceptor, while the latter were devoid of a
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