ライフサイエンスコーパス: hexamethonium

1 tinic receptor antagonists (mecamylamine and hexamethonium).

2 lfate and atropine methyl bromide but not by hexamethonium.

3 This effect was blocked by subconjunctival hexamethonium.

4 were mimicked by epibatidine and blocked by hexamethonium.

5 nsensitive to the general nicotinic blocker, hexamethonium.

6 d-tubocurarine > dihydro-beta-erythroidine > hexamethonium.

7 l Ringer solution or by bursts of stimuli in hexamethonium.

8 notoxin (0.1 microM), but were unaffected by hexamethonium (0.1 mM), suggesting that they result from

9 The authors found that hexamethonium (10 mg/kg) and propranolol (1 and 20 mg/kg

10 rvation before harvesting or rats were given hexamethonium (10 mg/kg, i.v.), a ganglionic blocking ag

11 (epibatidine, 10(-10) mol/L) or antagonist (hexamethonium, 10(-4) mol/L) of nAChRs as well as the po

12 Nicardipine, atropine, TTX, or hexamethonium (100 microM) also blocked the evoked peris

13 antagonists tetrodotoxin (TTX; 0.6 microM), hexamethonium (100 microM) or atropine (1 microM), when

14 Hexamethonium (100 microM) partly inhibited fEPSCs in 28

15 Hexamethonium (100 micromol/L) inhibited fEPSPs in the g

16 ) but not by the peripheral nAChR antagonist hexamethonium (15 micromol/kg, i.p.).

17 y the nicotinic receptor/ion channel blocker hexamethonium (150 microM).

18 cantly reduced by subdiaphragmatic vagotomy, hexamethonium (20 mg kg(-1)) and N (G)-nitro-L-arginine

19 s, preparations were treated with sufficient hexamethonium (200 microM) to block nicotinic responses

20 lockade of peripheral nicotinic receptors by hexamethonium (3 mg/kg, i.v.).

21 Hexamethonium (300 microM) added to the intermediate cha

22 Hexamethonium (300 microM) almost blocked the oral contr

23 All responses to distension were blocked by hexamethonium (300 microM) and tetrodotoxin (1 microM).

24 (TTX; 1 microM) abolished all sJPs, whereas hexamethonium (300 microM) either abolished, or substant

25 mulation or middle chambers, were blocked by hexamethonium (300 microM) in any chamber.

26 e were abolished by tetrodotoxin (1 microM), hexamethonium (300 microM) or atropine (1 microM), sugge

27 EJPs and IJPs were abolished by hexamethonium (300 microM) or tetrodotoxin (1 microM), b

28 hydro-beta-erythroidine (DHbetaE; 1 nM), and hexamethonium (300 microM) significantly inhibited ACh-i

29 ons in the LM and CM that were unaffected by hexamethonium (300 microM), but were reduced by yohimbin

30 Administration of hexamethonium (300 microM), to block sympathetic ganglio

31 This was blocked by hexamethonium (300 microM), which did not affect the tra

32 inistration of the ganglionic blocking agent hexamethonium (5 mg/kg) or an arginine vasopressin (AVP)

33 ent with the peripherally acting antagonist, hexamethonium (5 mg/kg), did not, indicating that c-fos

34 dose dependently, which was abolished by ICB hexamethonium (5 microg), thus suggesting that the atten

35 Hexamethonium (500 microM), decamethonium (500 microM),

36 d by atropine (100-200 microg kg-1), whereas hexamethonium (8 mg kg-1) had no effect.

37 Hexamethonium, a nonspecific nicotinic receptor antagoni

38 S-induced vasodilation was not attenuated by hexamethonium, an autonomic ganglion blocking agent, but

39 nic and muscarinic receptors were blocked by hexamethonium and atropine, 20 Hz stimulation for 10 s i

40 arterial pressure to the ganglionic blocker hexamethonium and decreased urinary norepinephrine level

41 ibited by the nicotinic receptor antagonists hexamethonium and dihydro-beta-erythroidine and reduced

42 Both i.v. hexamethonium and locally applied prazosin abolished the

43 e rate constants for block of alpha3beta4 by hexamethonium and of alpha3beta2 by mecamylamine were 1.

44 ension was significantly enhanced by L-NAME, hexamethonium and TTX.

45 serine; and mixed antagonism by pancuronium, hexamethonium, and d-tubocurarine.

46 e competitive antagonists, (+)-tubocurarine, hexamethonium, and dihydro-beta-erythroidine, only 2-15-

47 PSPs in second-order neurons were blocked by hexamethonium, and most slow EPSPs were blocked by an an

48 contrast, the nicotinic receptor antagonist, hexamethonium, and the N-type calcium channel toxin, ome

49 nduced Cl(-) secretion was decreased by TTX, hexamethonium, and the serosal FFA3 agonists acetate or

50 Mecamylamine, d-tubocurarine, and hexamethonium blocked the function by a noncompetitive m

51 Hexamethonium blocked the spread of label via nicotinic

52 Perfusion with hexamethonium bromide resulted in complete blockade of g

53 osure to cholinergic antagonists, curare and hexamethonium bromide, which block chemical neurotransmi

54 inhibited by the autonomic ganglion blocker hexamethonium bromide.

55 donor rats were pretreated with atropine or hexamethonium but not with guanethidine or vagotomy.

56 These local responses were observed in hexamethonium, but were blocked by ondansetron (5-HT(3)

57 (not obliterated) by D-tubocurarine (D-TC), hexamethonium (C6) and atropine.ACh, nicotine and piloca

58 nced in vivo by acute truncal vagotomy (TV), hexamethonium (C6), and NG-nitro-L-arginine methyl ester

59 thetic innervation with the ganglion blocker hexamethonium caused a 54% smaller decrease in blood pre

60 Hexamethonium caused equal lowering of MAP in RA+ mice a

61 Ganglionic blockade with hexamethonium caused greater fall in the BP of HS rats (

62 roidine, methyllycaconitine, d-tubocurarine, hexamethonium, decamethonium, and mecamylamine either fa

63 , in the remaining 87% of anal preparations, hexamethonium had no effect on the anal contraction of t

64 -intra-arterial infusions of tetrodotoxin or hexamethonium had no significant effect on the contracti

65 However, nicotinic antagonists, except hexamethonium, have comparable affinities for functional

66 The effects were blocked by 50 micromol/l hexamethonium (HEX).

67 or without the nAchR-nonspecific antagonist hexamethonium (HXM) (10(-5) M) for 72 hours.

68 ith or without nAchR non specific antagonist hexamethonium (HXM) (10(-5)M) for 72 hours.

69 osteric building blocks, both connected by a hexamethonium linker, we were able to prove a bitopic bi

70 ial (CAP), made submaximal by treatment with hexamethonium (O.4 mM), was used as an index of transmis

71 alpha3 AChRs were inhibited by hexamethonium or mecamylamine.

72 which was reduced by MQC, as well as by TTX, hexamethonium or removal of the submucosal plexus.

73 nse was similar despite reflex blockade with hexamethonium or volume reexpansion, indicating its inde

74 either blockade of ganglionic transmission (hexamethonium) or a drop in arterial blood pressure (nit

75 affected by selective blockers of nicotinic (hexamethonium) or serotonin (N-(1-azabicyclo-[2.2.2]oct-

76 rial pressure responses to administration of hexamethonium; P<0.05 vs. sham-operated SHR) and an impr

77 er before organ harvesting or treatment with hexamethonium prevented the effects of organ manipulatio

78 ) than nonpeptide antagonists (trimethaphan, hexamethonium, procaine, phencyclidine, cocaine, or clon

79 Oral and anal reflexes that were hexamethonium resistant were either abolished or attenua

80 CM, but was without effect on the transient hexamethonium-resistant anal relaxation.

81 Hexamethonium-resistant fEPSCs were inhibited by 97 +/-

82 Balloon distension elicited hexamethonium-resistant labeling of epithelial cells, in

83 ons stimulated with pulses of N2 or glucose, hexamethonium-resistant labeling of neurons occurred onl

84 Distension elicited hexamethonium-resistant pCREB immunoreactivity in calbin

85 Truncal vagotomy and administration of hexamethonium significantly reduced nonadrenergic, nonch

86 responses to cannabinoids in the presence of hexamethonium suggest further that CB(1) receptors occur

87 uroprotective effect by the ganglion blocker hexamethonium suggested a neurogenically mediated pathwa

88 ed preparations persisted in the presence of hexamethonium, suggesting that the deficit involved the

89 In the presence of hexamethonium, suramin (100 micromol/L) or the P2X antag

90 inability of pretreatment with atropine and hexamethonium to reduce the increases in hepatic vagal a

91 Early hexamethonium treatment attenuates acute excessive relea

92 After hexamethonium treatment, it was found that the acute hyp

93 In the remaining 85% of oral preparations, hexamethonium usually attenuated the oral contraction of

94 d atropine or after ganglionic blockade with hexamethonium, was not different between TG and WT mice.