ライフサイエンスコーパス: tachyphylaxis

1 cell signaling that are limited by receptor tachyphylaxis.

2 this partial agonist acted without inducing tachyphylaxis.

3 altered the kinetics of desensitization and tachyphylaxis.

4 as attenuated over time, suggesting possible tachyphylaxis.

5 ions in the TRPV1-ARD binding site eliminate tachyphylaxis.

6 plays an opposing role and is necessary for tachyphylaxis.

7 whether receptor trafficking contributes to tachyphylaxis.

8 a pivotal role in receptor sensitization vs. tachyphylaxis.

9 s of CRF were reproducible, and there was no tachyphylaxis.

10 ardial application of bradykinin demonstrate tachyphylaxis.

11 ncreasing beta(2)AR expression or minimizing tachyphylaxis.

12 injections of IL-12 do not induce a state of tachyphylaxis.

13 desensitize at a faster rate and attenuated tachyphylaxis.

14 cal use of certain MR agonists is limited by tachyphylaxis, a reduced responsiveness to repeated comp

15 Importantly, interruption of tachyphylaxis and bradyphylaxis restores cancer cell cyt

16 in most patients for up to 156 weeks without tachyphylaxis and had an acceptable safety profile.

17 Resistance reflects rapid (tachyphylaxis) and slow (bradyphylaxis) mechanisms of de

18 mpairment of normal inotropic and lusitropic tachyphylaxis, and exhibited accelerated development of

19 vels may play a very minor role in mediating tachyphylaxis; and 4) alterations in adiponectin recepto

20 agonist-induced TRPV1 desensitization and/or tachyphylaxis are still incompletely understood.

21 Motilin tachyphylaxis both in the presence or absence of tetrodo

22 st UP is blocked by alpha-beta methylene ATP tachyphylaxis, by reactive blue 2, and by apamin.

23 ary occlusion, 14 of 25 neurons demonstrated tachyphylaxis compared to 12 of 15 tested with bradykini

24 d response during constant Cap exposure) and tachyphylaxis (diminished response to successive applica

25 In neurons demonstrating tachyphylaxis, dorsal cervical cold block partially rest

26 llular solutions resulted in nearly complete tachyphylaxis even with intracellular Ca2+ buffered to l

27 c tissues nociception to bradykinin exhibits tachyphylaxis, however, this phenomenon has not been rig

28 P sorting cycle seemed to correlate with the tachyphylaxis-inducing properties of each compound, but

29 Tachyphylaxis is mediated by cGMP-dependent protein kina

30 One cause of tachyphylaxis is receptor desensitization, usually accom

31 response on repetitive drug exposure (i.e., tachyphylaxis) is a particular problem for the vasoconst

32 Tolerance and tachyphylaxis may occur, particularly with longer-term i

33 ely, desensitization of sst on tumor tissue (tachyphylaxis) may occur occasionally in patients on chr

34 Neither tachyphylaxis nor apparent toxicity has been noted.

35 Surprisingly, tachyphylaxis of increased local vascular permeability w

36 rmined if repeated challenges with BK led to tachyphylaxis of neurally mediated responses in subjects

37 Repeated BK challenges led to tachyphylaxis of sneezing and of neurally mediated serou

38 ll agonist, such as nicotine, produces rapid tachyphylaxis of the P20N40-measured sensory inhibition

39 does not result in the development of either tachyphylaxis or upregulation of sst as assessed by chan

40 We did not observe a tachyphylaxis phenomenon.

41 The principal findings were that (1) tachyphylaxis rapidly developed to the BJR-mediated hemo

42 d that this reduction was not an artifact of tachyphylaxis resulting from repeated administration of

43 eated coronary occlusions may also result in tachyphylaxis, thereby reducing cardiac sensation on sub

44 These findings suggest that tachyphylaxis to 5-HT(3) receptor agonists may be due to

45 utamol (0.3 to 3.5 nmol.min-1) did not cause tachyphylaxis to an identical repeated infusion after a

46 r factor regulating inotropic and lusitropic tachyphylaxis to beta-adrenergic agonist, which likely c

47 markedly attenuated after the development of tachyphylaxis to PBG in saline- and in L-NAME-treated ra

48 However, the rate of development of tachyphylaxis to PBG was markedly faster in the L-NAME-t

49 These findings suggest that tachyphylaxis to PBG was not due to the loss of central

50 Furthermore, the TREC did not display tachyphylaxis to prolonged agonist exposure (desensitiza

51 The tachyphylaxis to repeated coronary artery occlusions may

52 ificant and prolonged responses to 5-HT with tachyphylaxis to repeated injections.

53 dditional studies provided evidence that (1) tachyphylaxis to the 5-HT(3)R agonists was not due to im

54 progressive disease while on K may be due to tachyphylaxis to the adrenolytic properties of K.

55 The pronounced tachyphylaxis to the Bezold-Jarisch reflex (BJR) respons

56 hyl-5-HT were not responsible for preventing tachyphylaxis to the BJR reflex responses elicited by 5-

57 inhibition of NOS alters the development of tachyphylaxis to the BJR responses elicited by PBG in co

58 HT(2)R agonist, alpha-methyl-5-HT, prevented tachyphylaxis to the BJR-mediated hemodynamic responses

59 NAC response developed a profound tolerance/tachyphylaxis to the drug-induced increase in extracellu

60 improves insulin resistance in DIO mice; 3) "tachyphylaxis" to the effect of chronic MTII treatment o

61 the first transmembrane domain that confers tachyphylaxis upon ASIC2a.

62 Tachyphylaxis was hypothesized to account for the reduce

63 Tachyphylaxis was not observed.

64 diminished over the following 72 hours, the tachyphylaxis was reversible.

65 that chronic exposure to octreotide induces tachyphylaxis, we hypothesized that chronic exposure of

66 Both acute desensitization and tachyphylaxis were greatly diminished by reductions in e

67 to repeated applications of capsaicin, i.e., tachyphylaxis, while calmodulin plays an opposing role a

68 .d. SLIGRL-NH(2) for 9 min, to partial (25%) tachyphylaxis with repeated injection.