ライフサイエンスコーパス: capsazepine

1 d by ENaC delta subunit agonists (icilin and capsazepine).

2 uld be inhibited by the ion channel blocker, capsazepine.

3 d proliferation, which could be abrogated by capsazepine.

4 Transcription was not inhibited by capsazepine.

5 is effect is inhibited by the VR1 antagonist capsazepine.

6 or potential vanilloid subtype 1 antagonist, capsazepine.

7 mesenteric resistance arteries is blocked by capsazepine.

8 increased EPSC frequency, effects blocked by capsazepine.

9 mpletely blocked by the capsaicin antagonist capsazepine.

10 se, which could be blocked by the antagonist capsazepine.

11 was thus somewhat more potent (5-fold) than capsazepine.

12 or by the vanilloid VR1 receptor antagonist capsazepine.

13 d protons) with enhanced potency relative to capsazepine.

14 ium uptake in CHO cells lacking rVR1, unlike capsazepine.

15 cting 25- and 60-fold greater potencies than capsazepine.

16 current was suppressed by the VR1 antagonist capsazepine.

17 ich were reversibly antagonized by 10 microM capsazepine.

18 and were blocked by the capsaicin antagonist capsazepine.

19 but were unaffected by the TRPV1 antagonist capsazepine.

20 Capsazepine (1 microM) reduced the capsaicin-evoked memb

21 id agonist, was not significantly altered by capsazepine (10 and 30 mg/kg, i.p.) or SB 366791 (2 mg/k

22 Intraplantar injection of either capsazepine (10 microg) or SB 366791 (3 microg) attenuat

23 ntial discharge that was nearly abolished by capsazepine (10 microM) and inhibited by over 70 % with

24 The TRPV1 antagonist capsazepine (10 microm) significantly attenuated the ner

25 by a vanilloid receptor 1 (VR1) antagonist, capsazepine (10 microM), and was rapidly inactivating (a

26 the putative capsaicin receptor antagonist, capsazepine (10 microM).

27 Bath application of the TRPV1 antagonist capsazepine (10 mum) caused a significant attenuation of

28 The VR1 antagonist capsazepine (10-20 microm) attenuated CAP responses.

29 inhibit NO synthase; and (4) combined 20 mm capsazepine + 10 mm l-NAME.

30 ocked by the vanilloid receptor 1 antagonist capsazepine (100 microm).

31 was not antagonized by the TRPV1 antagonist, capsazepine; 2) ACEA significantly inhibited ( approxima

32 blockade of vanilloid (VR1) receptors using capsazepine (3 micromol/L) inhibited the responses.

33 , S(-)-raclopride (5 mg/kg, i.p.) but not by capsazepine (40 mg/kg, i.p.), a transient receptor poten

34 - 1 I.P.), by systemic TRPV1 antagonism with capsazepine(40mg kg-1 I.P.), or by systemic CB2 receptor

35 Initial peak in capsazepine (44 +/- 4%CVCmax), l-NAME (56 +/- 4%CVCmax)

36 or, TRPV1, because blockers of this channel, capsazepine (71.9+/-11.1% inhibition, n=9; P<0.001) and

37 l hyperaemia was significantly attenuated in capsazepine (73 +/- 6%CVCmax), l-NAME (47 +/- 5%CVCmax)

38 CCI animals was significantly attenuated by capsazepine, a blocker for both TRPM8 and TRPV1 (transie

39 and reversibly blocked by pretreatment with capsazepine, a competitive antagonist of the vanilloid t

40 Capsazepine, a potent antagonist of vanilloids, inhibite

41 altered by pretreatment with indomethacin or capsazepine, a selective antagonist of the transient rec

42 tivation, because the response is blocked by capsazepine, a selective TRPV1 antagonist.

43 andin receptor antagonist, but is blocked by capsazepine, a TRPV1 and TRPM8 receptor antagonist.

44 in control preparations by pretreatment with capsazepine, a TRPV1 antagonist, but not amiloride, a no

45 henium red, a VR1 ionophore blocker, but not capsazepine, a vanilloid antagonist indicating that cata

46 IL-8 releases were suppressed by exposure to capsazepine, AG 1478, ERK inhibitor PD 98059, p38 inhibi

47 in-related behaviours that were inhibited by capsazepine and absent in TRPV1-null animals.

48 in the presence of the competitive inhibitor capsazepine and in a capsaicin-insensitive point mutant.

49 uppressed by the TRPV1-selective antagonists capsazepine and JYL 1421.

50 response was antagonized by the antagonists capsazepine and ruthenium red.

51 iferatoxin and capsaicin), VR-1 antagonists (capsazepine and SB-366791), and at elevated temperatures

52 d by ruthenium red and the TRPV1 antagonists capsazepine and SB-366791.

53 420 nm and 540 nm, and could be inhibited by capsazepine and SKF96365, which also inhibited osteogeni

54 3-yl)-N-(1H-indol-6-yl)acrylamide (AMG0610), capsazepine, and (2E)-3-(4-chlorophenyl)-N-(3-methoxyphe

55 sed by blue/green could also be abrogated by capsazepine, and by the antioxidant, N-acetylcysteine.

56 s were fully blocked by the TRPV1 inhibitor, capsazepine, and no responses to OEA were observed in ne

57 itive cells, inhibited by the TRPV1 blocker, capsazepine, and occurred in a PKC-dependent manner.

58 nyl-acetate 13-acetate 20-homovanillate) and capsazepine between human and rat TRPV1.

59 Capsazepine blocked the response of TG neurons to piperi

60 TRPV1 antagonists, 5'-iodoresiniferatoxin or capsazepine, but was not altered by the cannabinoid type

61 istration of the TRPv1 receptor antagonists, capsazepine (Capz; 100 microg/100 microl), iodoresinafer

62 with effects suppressed by TRPV1 antagonists capsazepine (CPZ) and BCTC ((4-(3-chloro-2-pyridinyl)-N-

63 croinjection of a TRPV1 receptor antagonist (capsazepine) did not affect post-ictal analgesia in GEPR

64 Capsazepine had no effect on the sustained proton-induce

65 rofoundly suppressed by the TRPV1 antagonist capsazepine, in hearts of TRPV1 knockout mice compared w

66 gonist capsazepine with the magnitude of the capsazepine-induced reductions being greater in SHR than

67 he competitive vanilloid receptor antagonist capsazepine inhibited [(3)H]RTX binding to HEK293/VR1 ce

68 Likewise, the competitive antagonist capsazepine inhibited RTX-induced desensitization with p

69 +/- 6%CVCmax), l-NAME (47 +/- 5%CVCmax) and capsazepine + l-NAME (31 +/- 7%CVCmax) sites compared to

70 +/- 4%CVCmax), l-NAME (56 +/- 4%CVCmax) and capsazepine + l-NAME (32 +/- 6%CVCmax) sites was signifi

71 n was suppressed by preincubating HCECs with capsazepine, matrix metalloproteinase 1 (MMP1) inhibitor

72 channels with many TRPV1 antagonists such as capsazepine, N-(4-tertiarybutylphenyl)-4-(3-chloropyridi

73 stingly, the rate of activation and block by capsazepine of RTX-induced currents are significantly sl

74 ure a], with enhanced activity compared with capsazepine on rat VR1 expressed in Chinese hamster ovar

75 lished by pretreatment with methazolamide or capsazepine or by dimethyl amiloride coperfusion.

76 Inhibition of TRPV1 by capsazepine or ruthenium red reduced the apoptosis, impl

77 The TRPV1 receptor antagonists, capsazepine or SB 366791, were applied to the RF to dete

78 were attenuated by pre-treatment with either capsazepine or SB 366791.

79 r benzolamide, vanilloid receptor antagonist capsazepine, or sodium-hydrogen exchanger 1 (NHE-1) inhi

80 The TRPV1 receptor antagonist capsazepine prevented the increased cough sensitivity in

81 In contrast, the TRPV1 antagonist capsazepine produces the opposite effects.

82 In the presence of capsazepine, responses to the mixture of piperine and pr

83 B597 increased AEA-evoked cobalt uptake in a capsazepine-sensitive manner.

84 n of external pH from 7.4 to 6.4 activated a capsazepine-sensitive outwardly rectifying membrane curr

85 Capsazepine showed only weak antagonism for both pH and

86 also insensitive to AM630 and unaffected by capsazepine suggesting that neither CB2 nor TRPV1 recept

87 ibited by the vanilloid receptor antagonist, capsazepine, suggesting they do not arise from the activ

88 l + 10% lactated Ringer solution); (2) 20 mm capsazepine to inhibit TRPV-1 channels; (3) 10 mm l-NAME

89 ific [3H]RTX binding, whereas the potency of capsazepine was approximately 10-fold higher for inhibit

90 inistration of the TRPv1 receptor antagonist capsazepine with the magnitude of the capsazepine-induce