ライフサイエンスコーパス: alpha(1) agonist

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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 l intra-arterial infusions of phenylephrine (alpha(1)-agonist) and dexmedetomidine (alpha(2)-agonist)

6 o 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 Midodrine is an alpha1-agonist approved for orthostatic hypotension.

13 erestingly, LTD can be induced when M(1) and alpha1 agonists are coapplied at concentrations too low

14 er cells, LNCaP, to either quinazoline-based alpha1-agonist by androgens.

15 An alpha1-agonist could not substitute for epinephrine in p

16 noclonal antibody to Galphah/Tg reveals that alpha1-agonist deprivation during culture of VZ cells in

17 ntra-arterial infusion of phenylephrine (PE; alpha(1) -agonist) during (i) infusion of an endothelium

18 ntra-arterial infusion of phenylephrine (PE; alpha1 -agonist) during ATP or control vasodilatator inf

19 Methoxamine (10(-9) to 10(-5) mol/L, an alpha1-agonist) had no effect, whereas U44619, a thrombo

20 ulation combined with alpha2 antagonists and alpha1 agonists in a mixture to reinstate neonatal level

21 ion of CPI-17 Thr38 and MYPT1 Thr853, during alpha(1) agonist-induced contraction with/without variou

22 (2+) release, Ca(2+) influx, PKC and ROCK in alpha(1)-agonist-induced contraction and phosphorylation

23 f alpha(1A) receptors, plays a major role in alpha(1)-agonist-induced contraction of small resistance

24 onstriction with different vasoconstrictors (alpha1-agonist methoxamine, endothelin [ET-1], phorbol e

25 The response of patients to the alpha1-agonist midodrine supports the hypothesis of part

26 -agonist) and phenylephrine (PE, a selective alpha1-agonist) on spontaneous and D,L-homocysteic acid

27 d little Ca(2+) sensitization in response to alpha(1)-agonist or endothelin-1.

28 tra-arterial infusions of phenylephrine (PE; alpha(1)-agonist) or NPY (Y1R-agonist) during: (1) intra

29 In control slices, bath application of the alpha(1)-agonist phenylephrine (PHE; 10 microM) depolari

30 -agonist oxymetazoline (5 microM), while the alpha1-agonist phenylephrine (100 microM) caused only a

31 s) challenged with a dose-response using the alpha1-agonist phenylephrine (PE), with and without the

32 ulated during intraarterial infusions of the alpha1-agonist phenylephrine and the alpha2-agonist clon

33 entricular zone (VZ) germinal cells with the alpha1-agonist phenylephrine during development in vitro

34 ceptor agonist, octopamine, and the specific alpha(1) agonist, phenylephrine, increased alveolar flui

35 pamezole) receptors or of either the partial alpha(1)-agonist, phenylephrine, or full alpha(2)-agonis

36 ss sensitive to metabolic inhibition than an alpha1-agonist, phenylephrine (PE), in the exercising hu

37 NE, the beta-agonist, isoproterenol, or the alpha1-agonist, phenylephrine, were infused into the MPO

38 ncreasing IUP over MAP than the nonselective alpha(1)-agonists phenylpropanolamine (PPA) (1) and ST-1

39 l dysautonomia and indicates that the use of alpha1-agonists to pharmacologically replace lower-extre

40 In contrast, phenylephrine contractions (alpha(1) agonist) were enhanced in Aff from AngII-infuse