ライフサイエンスコーパス: BAY K 8644

1 ere exposed to the L-type channel agonist +/-BAY K 8644.

2 L-type calcium channel agonists FPL 64176 or Bay K 8644.

3 the 1,4-dihydropyridine receptor agonist +/-Bay K 8644.

4 ed by the L-type Ca(2+) channel opener, S(-)-Bay K 8644.

5 dihydropyridine L-type Ca2+ channel agonist, Bay K 8644.

6 t by nimodipine and cadmium and augmented by Bay K 8644.

7 se responses were enhanced with LTCC agonist Bay-K-8644.

8 S-(-)-Bay K 8644 (1 microM) enhanced calcium channel currents

9 markedly reduced the outward current, while Bay K 8644 (1 microM) enhanced it.

10 When slow waves were enhanced with Bay K 8644 (1 microM), VIP decreased slow wave duration

11 n (10 mumol/L) of 8-bromo-cAMP but not by (-)Bay K 8644 (1 mumol/L).

12 H-pyrrole-3-carboxylic acid methylester) and Bay K 8644 ((+/-)-1,4-dihydro-2,6-dimethyl-5-nitro-4-[2-

13 Bay K 8644 (10 microM), an L-type Ca(2+) agonist, signif

14 milar constriction with l-NNA (50 microM) or Bay K 8644 (10 nM) did not.

15 ted Ca(V)1.2 channels were supramodulated by BAY K 8644 (10-fold increase) compared to control channe

16 Bay K 8644 (100 nmol/L) increased the spark frequency by

17 roM) always partially inhibited currents and Bay K 8644 (2-5 microM) always enhanced currents, indica

18 esponse to the L-type Ca(2+) channel agonist BAY K 8644 (300 nmol/kg), suggesting that CaM kinase-ind

19 t of light on AANAT activity was reversed by Bay K 8644, 8Br-cAMP, and the proteasome inhibitor lacta

20 l Ca2+ transport (nitrendipine, nisoldipine, Bay K 8644, A 23187) do not significantly alter either I

21 ype voltage-gated channels, and augmented by Bay K 8644, a Ca(2+) channel agonist.

22 reduced significantly vasopressor effects to BAY K 8644, a calcium-channel opener, attenuated signifi

23 It is concluded that Bay K 8644 activates SR Ca2+ release at rest, independen

24 st, depolarization of cells by high K(+) and Bay K 8644, an L-type Ca(2+) channel agonist, inhibited

25 Bay K 8644, an L-type Ca(2+) channel agonist, initiated

26 Bay K 8644, an L-type Ca2+ channel agonist, was shown pr

27 ame voltage range in the absence of ISO with Bay K 8644 and FPL 64176 (n=9).

28 lly increased by the calcium channel agonist Bay K 8644 and inhibited by the calcium channel blocker

29 ductance channel (20-23 pS) was sensitive to Bay K 8644 and is presumed to represent L-type calcium c

30 r repolarization in the presence of 1 microM Bay K 8644 and were resistant to omegaCGVIA.

31 The influence of a calcium agonist (BAY K 8644) and calcium blockers on (+)- and (-)-epibati

32 The known actions of (+/-)Bay K 8644 as an L type calcium channel agonist, the rep

33 oproterenol (ISO), dibutyryl-cAMP (db-cAMP), Bay K 8644 (BayK), Okadaic acid (OA, a phosphatase inhib

34 sensitivity to dihydropyridines (nimodipine, Bay K 8644), benzothiazepines (diltiazem) and acetonitri

35 V)1.2 channels can be selectively rescued by BAY K 8644 but not protein kinase A-dependent phosphoryl

36 lls increased proportionately in response to Bay K 8644, but the maximal current density was still lo

37 The self-biting provoked by (+/-)Bay K 8644 can be inhibited by pretreating the mice with

38 Z-VAD); at higher insult levels (1000 microM+Bay K 8644), cells underwent necrosis insensitive to Z-V

39 ovoked by injecting small quantities of (+/-)Bay K 8644 directly into the lateral ventricle of the br

40 pine, verapamil, diltiazem, and the agonist, Bay K 8644, even at relatively high concentrations.

41 Bay K 8644 evoked concentration-dependent reductions in

42 usion of Ca(2+)-free solution, nifedipine or Bay K 8644, excluding the direct involvement of voltage-

43 fedipine, cadmium, verapamil), and agonists (Bay K 8644, FPL 64176) were used to separate SMC from I(

44 ta from 35 other cells exposed to 500 nmol/L Bay K 8644 gave a slope of 0.0041 nS x pF(-1) x mm Hg(-1

45 In lipid bilayers, Bay K 8644 had no effect on either single-channel curren

46 The L type calcium channel agonist (+/-)Bay K 8644 has been reported to cause characteristic mot

47 yl]pyridine-3-carboxyli c acid methyl ester (Bay K 8644) has a similar action.

48 = approximately 23 ms) that were enhanced by Bay K 8644, in addition to the brief openings (tau(o) =

49 Conversely, the DHP agonist Bay K 8644 increased both I(Ca) and DeltaC(m) amplitude

50 y Ca2+ response to 100 pM Ang II by 49%, and BAY K 8644 increased oscillation frequency by 86%, or ca

51 From Fura-2 emissions we determined that +/-BAY K 8644 induced a rapid (<2 min) and persistent incre

52 ectively prevented protein kinase A- but not BAY K 8644-induced prolongation of the cardiac action po

53 inhibition of protein kinase C did not block Bay-K 8644-induced ERK activation.

54 as well as those observed in the presence of Bay K 8644, NMDA, or tetraethylammonium were abolished i

55 This suggests that the effect of Bay K 8644 on Ca2+ sparks is mediated by the sarcolemmal

56 Here, the effects of Bay K 8644 on local SR Ca2+ release events (Ca2+ sparks)

57 cation of the L-type calcium channel agonist Bay K 8644 or activation of NMDA receptors enhanced plat

58 to increasing bath concentrations of either Bay K 8644 or K+.

59 )-epibatidine was significantly increased by BAY K 8644 pretreatment.

60 otassium or with the calcium channel agonist Bay K 8644 protected neurons.

61 Exposure to +/-BAY K 8644 resulted in a rapid (<2 min) increase (40%) i

62 ell L-type calcium channels with the agonist Bay-K 8644 resulted in phosphorylation of ERK and induct

63 < 0.05) larger than the enhancement by S-(-)-Bay K 8644 that was seen with cells incubated under iden

64 Bay K 8644, the L-type Ca2+ channel activator, increased

65 nel current and reduces the ability of S-(-)-Bay K 8644 to enhance this current, indicating that it i

66 The effect of Bay K 8644 was antagonized by the adenylyl cyclase inhib

67 This potentiation by BAY K 8644 was blocked by pretreating the animals with n

68 increase in Ca2+ spark frequency induced by Bay K 8644 was not affected by superfusion with Ca2+-fre

69 y roscovitine and by the L-channel activator Bay K 8644 was not occluded but additive.

70 ts responded to 1 nM Bay K 8644 while 100 nM Bay K 8644 was required to contract arterioles from diab

71 the activation of L-type calcium channels by BAY-K 8644 was unchanged during iloprost treatment.

72 )[III-IVa] was accentuated by exposure to +/-Bay K 8644, which caused a much larger hyperpolarizing s

73 arterioles from Sham rats responded to 1 nM Bay K 8644 while 100 nM Bay K 8644 was required to contr

74 t lower insult levels (200 micrometer Zn(2+)+Bay K 8644), Zn(2+)-induced death appeared apoptotic und