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1 when treated with indiplon, a GABAA receptor alpha1 agonist.
2 not after administration of beta1, beta2, or alpha1 agonists.
3       In this model, epinephrine through its alpha1-agonist action had adverse effects on cerebral mi
4                         Agonists, such as an alpha(1)-agonist and endothelin-1, produced significant
5 o intra-arterial infusions of phenylephrine (alpha(1)-agonist) and dexmedetomidine (alpha(2)-agonist)
6 l intra-arterial infusions of phenylephrine (alpha(1)-agonist) and dexmedetomidine (alpha(2)-agonist)
7 us noradrenaline release), phenylephrine (an alpha1 agonist) and clonidine (an alpha2 agonist) in 10
8 enous noradrenaline release), phenylephrine (alpha1-agonist) and clonidine (alpha2-agonist) were asse
9  noradrenaline (NA) release), phenylephrine (alpha1-agonist) and dexmedetomidine (alpha2-agonist) wer
10 genous NE release), phenylephrine (selective alpha1-agonist), and clonidine (alpha2-agonist) were det
11  survival is reduced following withdrawal of alpha1-agonist, and support the hypothesis that Tg/Galph
12 erestingly, LTD can be induced when M(1) and alpha1 agonists are coapplied at concentrations too low
13 er cells, LNCaP, to either quinazoline-based alpha1-agonist by androgens.
14                                           An alpha1-agonist could not substitute for epinephrine in p
15 noclonal antibody to Galphah/Tg reveals that alpha1-agonist deprivation during culture of VZ cells in
16 ntra-arterial infusion of phenylephrine (PE; alpha1 -agonist) during ATP or control vasodilatator inf
17      Methoxamine (10(-9) to 10(-5) mol/L, an alpha1-agonist) had no effect, whereas U44619, a thrombo
18 ulation combined with alpha2 antagonists and alpha1 agonists in a mixture to reinstate neonatal level
19 ion of CPI-17 Thr38 and MYPT1 Thr853, during alpha(1) agonist-induced contraction with/without variou
20 (2+) release, Ca(2+) influx, PKC and ROCK in alpha(1)-agonist-induced contraction and phosphorylation
21 f alpha(1A) receptors, plays a major role in alpha(1)-agonist-induced contraction of small resistance
22 onstriction with different vasoconstrictors (alpha1-agonist methoxamine, endothelin [ET-1], phorbol e
23              The response of patients to the alpha1-agonist midodrine supports the hypothesis of part
24 -agonist) and phenylephrine (PE, a selective alpha1-agonist) on spontaneous and D,L-homocysteic acid
25 d little Ca(2+) sensitization in response to alpha(1)-agonist or endothelin-1.
26   In control slices, bath application of the alpha(1)-agonist phenylephrine (PHE; 10 microM) depolari
27 -agonist oxymetazoline (5 microM), while the alpha1-agonist phenylephrine (100 microM) caused only a
28 s) challenged with a dose-response using the alpha1-agonist phenylephrine (PE), with and without the
29 ulated during intraarterial infusions of the alpha1-agonist phenylephrine and the alpha2-agonist clon
30 entricular zone (VZ) germinal cells with the alpha1-agonist phenylephrine during development in vitro
31 ceptor agonist, octopamine, and the specific alpha(1) agonist, phenylephrine, increased alveolar flui
32 pamezole) receptors or of either the partial alpha(1)-agonist, phenylephrine, or full alpha(2)-agonis
33 ss sensitive to metabolic inhibition than an alpha1-agonist, phenylephrine (PE), in the exercising hu
34  NE, the beta-agonist, isoproterenol, or the alpha1-agonist, phenylephrine, were infused into the MPO
35 ncreasing IUP over MAP than the nonselective alpha(1)-agonists phenylpropanolamine (PPA) (1) and ST-1
36 l dysautonomia and indicates that the use of alpha1-agonists to pharmacologically replace lower-extre
37     In contrast, phenylephrine contractions (alpha(1) agonist) were enhanced in Aff from AngII-infuse

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