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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.
6 fect of external calcium ions (Ca2+o) on the alpha1-adrenoceptor-activated non-selective cation curre
9 e findings are consistent with the view that alpha1-adrenoceptors affect memory storage by modulating
10 e), and after 2 min of phenylephrine (PE; an alpha1 -adrenoceptor agonist) infusion via brachial arte
11 ntra-arterial infusion of phenylephrine (PE; alpha1 -adrenoceptor agonist) were calculated during (1)
12 n of beta2-adrenergic receptors, whereas the alpha1 adrenoceptor agonist methoxamine induces cerebral
14 cord transection (C2) and suppressed by the alpha1-adrenoceptor agonist phenylephrine, indicating th
15 ves, previously associated with bath-applied alpha1-adrenoceptor agonists, were not initially present
22 jor contraction through mechanisms involving alpha1-adrenoceptors and which are associated with propa
23 nsity and protein expression of alpha1A- and alpha1D-adrenoceptors, and increased cell surface expres
24 pendent of: (a) their capacity to antagonize alpha1-adrenoceptors; and (b) the hormone sensitivity st
25 amin, but they are totally unaffected by the alpha1 adrenoceptor antagonist prazosin or by capsaicin
26 h attenuated markedly in the presence of the alpha1 adrenoceptor antagonist, prazosin, or the MAP kin
27 dies documented that the quinazoline-derived alpha1-adrenoceptor antagonist doxazosin affects the att
30 n 0.2 microliter) alone or together with the alpha1-adrenoceptor antagonist prazosin (0.2 nmol) immed
31 twitch that remained in the presence of the alpha1-adrenoceptor antagonist prazosin (100 nM), showin
35 lls, whereas tamsulosin, a sulfonamide-based alpha1-adrenoceptor antagonist, was ineffective in induc
36 significance in the use of quinazoline-based alpha1-adrenoceptor antagonists (already in clinical use
37 apoptotic activity of the quinazoline-based alpha1-adrenoceptor antagonists (doxazosin and terazosin
38 ce from our laboratory has demonstrated that alpha1-adrenoceptor antagonists doxazosin and terazosin
42 evidence suggests that the quinazoline-based alpha1-adrenoceptor antagonists, doxazosin and terazosin
43 investigated the biological action of three alpha1-adrenoceptor antagonists, doxazosin, terazosin, a
44 e foot-withdrawal response, but in contrast, alpha1-adrenoceptors appear to mediate part of the antin
45 dications containing oxymetazoline (OXY), an alpha1-adrenoceptor (AR) agonist of the imidazoline clas
46 previously demonstrated that stimulation of alpha1-adrenoceptors (AR) causes hypertrophy of vascular
47 ed by atropine and were decreased by 65 % by alpha1-adrenoceptor blockade or spinal cord transection.
48 efficacy of other combinations, for example, alpha1-adrenoceptor blocker and 5alpha-reductase inhibit
50 ave shown that both antimuscarinic drugs and alpha1-adrenoceptor blockers can be useful for treatment
51 ymptoms, combinations of antimuscarinics and alpha1-adrenoceptor blockers have produced the most prom
52 ase 5 inhibitors seems to be as effective as alpha1-adrenoceptor blockers in male lower urinary tract
53 r the past years new formulations of several alpha1-adrenoceptor blockers were introduced to the mark
55 brain, with significant, regional-dependent alpha1 adrenoceptor cross-reactivity, limiting its poten
58 ptor-binding techniques were used to measure alpha1-adrenoceptor density and the affinity of CUMI-101
60 number of alpha1-adrenoceptors (or alpha1A + alpha1D-adrenoceptors) did not differ significantly betw
61 man prostate cancer cells, DU-145 (that lack alpha1-adrenoceptor), did not alter the ability of prost
62 enoxybenzamine, an irreversible inhibitor of alpha1-adrenoceptors, does not abrogate the apoptotic ef
64 ecreased both mineralocorticoid receptor and alpha1-adrenoceptor expressions within 5 hours in human
65 rodimerization did not alter the affinity of alpha1-adrenoceptors for norepinephrine, prazosin, or su
68 e contamination of (11)C-CUMI-101 binding to alpha1-adrenoceptors in human cerebellum under in vivo c
69 ed these findings and determined the role of alpha1-adrenoceptors in mediating the antinociceptive ef
70 esent study examined whether inactivation of alpha1-adrenoceptors in the BLA would alter the dose-res
72 ce apoptosis in prostate cancer cells via an alpha1-adrenoceptor-independent pathway, involving activ
76 (caspase cleavage-mediated) and reversible (alpha1 adrenoceptor-mediated) forms of channel activatio
77 ordings of 5-HT neurons revealed that, while alpha1-adrenoceptor-mediated excitation was unchanged, e
80 ized by decreased venous sensitivity to both alpha1-adrenoceptor-mediated vasoconstriction and beta2-
81 scription-polymerase chain reaction revealed alpha1D-adrenoceptor mRNA within pterygopalatine ganglia
82 sting that stimulation of NAD(P)H oxidase by alpha1-adrenoceptor occupation precedes HB-EGF release.
83 ward current, the outward current induced by alpha1 adrenoceptors often consisted of multiple peaks.
85 ngs indicate that activation of postsynaptic alpha1-adrenoceptors potentiates beta-adrenoceptor-media
90 expression and pharmacological properties of alpha1-adrenoceptor subtypes was examined using coimmuno
92 take in human cerebellum reflects binding to alpha1-adrenoceptors, suggesting that the cerebellum is
93 rs, and increased cell surface expression of alpha1D-adrenoceptors, suggesting a functional role for
97 rate subtype-selective heterodimerization of alpha1-adrenoceptors, which does not change their pharma
98 Conversely, coexpression of alpha1A-with alpha1D-adrenoceptors, which did not heterodimerize, had
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