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1 ivated macrophages, which was independent of alpha1 adrenoceptors.
2 motility, and pigmentation via the beta2 and alpha1 adrenoceptors.
3 independent of their capacity to antagonize alpha1-adrenoceptors.
4 eptive effects of morphine were modulated by alpha1-adrenoceptors.
5 g E(2) and P facilitation of lordosis is the alpha(1)-adrenoceptor.
7 fect of external calcium ions (Ca2+o) on the alpha1-adrenoceptor-activated non-selective cation curre
10 e findings are consistent with the view that alpha1-adrenoceptors affect memory storage by modulating
11 cubated with norepinephrine or the selective alpha(1)-adrenoceptor agonist phenylephrine, cGMP accumu
12 ng intra-BLA infusions of either cirazoline (alpha(1)-adrenoceptor agonist) or 8-br-cAMP (cAMP analog
14 e), and after 2 min of phenylephrine (PE; an alpha1 -adrenoceptor agonist) infusion via brachial arte
15 ntra-arterial infusion of phenylephrine (PE; alpha1 -adrenoceptor agonist) were calculated during (1)
16 n of beta2-adrenergic receptors, whereas the alpha1 adrenoceptor agonist methoxamine induces cerebral
18 cord transection (C2) and suppressed by the alpha1-adrenoceptor agonist phenylephrine, indicating th
19 ves, previously associated with bath-applied alpha1-adrenoceptor agonists, were not initially present
20 ation, and desensitization properties of the alpha(1)-adrenoceptor (alpha(1)-AR) subtypes conjugated
26 of an allosteric inhibitor pharmacophore for alpha(1)-adrenoceptors and mechanistic insight and a new
27 drenaline enhances I(Cl(swell)) by acting on alpha(1)-adrenoceptors and reduces I(Cl(swell)) by stimu
28 increases nociception through the action of alpha(1)-adrenoceptors and the other inhibits nociceptio
33 jor contraction through mechanisms involving alpha1-adrenoceptors and which are associated with propa
34 pendent of: (a) their capacity to antagonize alpha1-adrenoceptors; and (b) the hormone sensitivity st
37 onse was not significantly attenuated by the alpha(1)-adrenoceptor antagonist prazosin (500 nM), indi
38 -cGMP reverses the inhibitory effects of the alpha(1)-adrenoceptor antagonist prazosin on lordosis be
39 ort-term diabetes was assessed by evaluating alpha(1)-adrenoceptor antagonist prazosin on NBF, MNC, a
40 ased I(Cl(swell)) and in the presence of the alpha(1)-adrenoceptor antagonist prazosin, noradrenaline
41 2)-adrenoceptor antagonist yohimbine nor the alpha(1)-adrenoceptor antagonist WB4101 altered latencie
42 Rp-cAMPS (cAMP inhibitor), but not prazosin (alpha(1)-adrenoceptor antagonist), blocked CRF(6-33)-ind
43 achial artery administration of prazosin (an alpha(1)-adrenoceptor antagonist), yohimbine (an alpha(2
44 amin, but they are totally unaffected by the alpha1 adrenoceptor antagonist prazosin or by capsaicin
45 h attenuated markedly in the presence of the alpha1 adrenoceptor antagonist, prazosin, or the MAP kin
46 dies documented that the quinazoline-derived alpha1-adrenoceptor antagonist doxazosin affects the att
49 n 0.2 microliter) alone or together with the alpha1-adrenoceptor antagonist prazosin (0.2 nmol) immed
50 twitch that remained in the presence of the alpha1-adrenoceptor antagonist prazosin (100 nM), showin
54 lls, whereas tamsulosin, a sulfonamide-based alpha1-adrenoceptor antagonist, was ineffective in induc
55 significance in the use of quinazoline-based alpha1-adrenoceptor antagonists (already in clinical use
56 apoptotic activity of the quinazoline-based alpha1-adrenoceptor antagonists (doxazosin and terazosin
57 ce from our laboratory has demonstrated that alpha1-adrenoceptor antagonists doxazosin and terazosin
61 evidence suggests that the quinazoline-based alpha1-adrenoceptor antagonists, doxazosin and terazosin
62 investigated the biological action of three alpha1-adrenoceptor antagonists, doxazosin, terazosin, a
63 e foot-withdrawal response, but in contrast, alpha1-adrenoceptors appear to mediate part of the antin
65 dications containing oxymetazoline (OXY), an alpha1-adrenoceptor (AR) agonist of the imidazoline clas
66 previously demonstrated that stimulation of alpha1-adrenoceptors (AR) causes hypertrophy of vascular
69 ed by atropine and were decreased by 65 % by alpha1-adrenoceptor blockade or spinal cord transection.
70 efficacy of other combinations, for example, alpha1-adrenoceptor blocker and 5alpha-reductase inhibit
72 ave shown that both antimuscarinic drugs and alpha1-adrenoceptor blockers can be useful for treatment
73 ymptoms, combinations of antimuscarinics and alpha1-adrenoceptor blockers have produced the most prom
74 ase 5 inhibitors seems to be as effective as alpha1-adrenoceptor blockers in male lower urinary tract
75 r the past years new formulations of several alpha1-adrenoceptor blockers were introduced to the mark
78 brain, with significant, regional-dependent alpha1 adrenoceptor cross-reactivity, limiting its poten
81 ptor-binding techniques were used to measure alpha1-adrenoceptor density and the affinity of CUMI-101
84 man prostate cancer cells, DU-145 (that lack alpha1-adrenoceptor), did not alter the ability of prost
85 enoxybenzamine, an irreversible inhibitor of alpha1-adrenoceptors, does not abrogate the apoptotic ef
87 ecreased both mineralocorticoid receptor and alpha1-adrenoceptor expressions within 5 hours in human
88 rodimerization did not alter the affinity of alpha1-adrenoceptors for norepinephrine, prazosin, or su
89 contribute more to basal vascular tone than alpha(1)-adrenoceptors in the forearms of young healthy
90 t studies, we tested the hypotheses that (1) alpha(1)-adrenoceptors in the HYP enhance lordosis respo
92 e contamination of (11)C-CUMI-101 binding to alpha1-adrenoceptors in human cerebellum under in vivo c
93 ed these findings and determined the role of alpha1-adrenoceptors in mediating the antinociceptive ef
94 esent study examined whether inactivation of alpha1-adrenoceptors in the BLA would alter the dose-res
96 ce apoptosis in prostate cancer cells via an alpha1-adrenoceptor-independent pathway, involving activ
101 hatase inhibition are critically involved in alpha(1)-adrenoceptor-mediated vascular smooth muscle co
102 (caspase cleavage-mediated) and reversible (alpha1 adrenoceptor-mediated) forms of channel activatio
103 ordings of 5-HT neurons revealed that, while alpha1-adrenoceptor-mediated excitation was unchanged, e
106 ized by decreased venous sensitivity to both alpha1-adrenoceptor-mediated vasoconstriction and beta2-
107 sting that stimulation of NAD(P)H oxidase by alpha1-adrenoceptor occupation precedes HB-EGF release.
108 ward current, the outward current induced by alpha1 adrenoceptors often consisted of multiple peaks.
109 pathway mediates the facilitatory effects of alpha(1)-adrenoceptors on lordosis behavior in female ra
111 ngs indicate that activation of postsynaptic alpha1-adrenoceptors potentiates beta-adrenoceptor-media
112 expression and promotes IGF-I enhancement of alpha(1)-adrenoceptor potentiation of cAMP accumulation
114 antagonist prazosin, and are mimicked by the alpha(1)-adrenoceptor-selective agonist phenylephrine.
115 versed with wash, are largely blocked by the alpha(1)-adrenoceptor-selective antagonist prazosin, and
116 nger vasoconstriction evoked by extraluminal alpha(1)-adrenoceptor stimulation is blunted by vasodila
121 gical profile at both 5-HT(1A) receptors and alpha(1)-adrenoceptor subtypes was measured by binding a
124 expression and pharmacological properties of alpha1-adrenoceptor subtypes was examined using coimmuno
126 take in human cerebellum reflects binding to alpha1-adrenoceptors, suggesting that the cerebellum is
128 -cGMP signaling pathway, and (2) coupling of alpha(1)-adrenoceptors to this signal transduction pathw
130 me tonic force, MLCK FRET ratio activated by alpha(1)-adrenoceptors was approximately 60% of that act
132 rate subtype-selective heterodimerization of alpha1-adrenoceptors, which does not change their pharma
133 verall reduction of in vitro affinity at the alpha(1)-adrenoceptor while both potency and efficacy we
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