ライフサイエンスコーパス: prazosin

1 ceived alpha-blockers (chlorpromazine and/or prazosin).

2 h combat PTSD who are likely to benefit from prazosin.

3 could be blocked with an alpha-1 antagonist, prazosin.

4 in (Na/K)-ATP-ase activity were affected by prazosin.

5 controls, and this decrease was prevented by prazosin.

6 e (ERK), which was reduced by treatment with prazosin.

7 rats, and this reduction was ameliorated by prazosin.

8 h hydrochlorothiazide than with captopril or prazosin.

9 clonidine, diltiazem (sustained release), or prazosin.

10 nse was blocked by the alpha 1-AR antagonist prazosin.

11 cells with the alpha1-adrenergic antagonist prazosin.

12 fully inhibited by the alpha 1-AR antagonist prazosin.

13 alol, and the alpha1-adrenoceptor antagonist prazosin.

14 effect was abolished by propranolol but not prazosin.

15 affected by the alpha1-adrenergic antagonist prazosin.

16 blocked by the alpha 1-adrenergic antagonist prazosin.

17 oxantrone or the fluorescent compound BODIPY-prazosin.

18 ly 70% in the efflux activity of only BODIPY-prazosin.

19 having PTSD who received a prescription for prazosin.

20 ir ability to efflux mitoxantrone and BODIPY-prazosin.

21 oin (IAAP), an analogue of the Pgp substrate prazosin.

22 ment with the alpha1-adrenoceptor antagonist prazosin (0.1 mg/kg i.v.) before cocaine and lipopolysac

23 The alpha1-adrenergic receptor antagonist prazosin (0.1 microM) blocked the effects of NA on Ito,

24 ence of the alpha(1)-adrenoceptor antagonist prazosin (0.1 microm) vasoconstrictions at 90 mmHg were

25 the alpha(1)-adrenergic receptor antagonist, prazosin (0.1 microm), blocked constrictions in MV but n

26 cromol/L), NE+propranolol (2 micromol/L), NE+prazosin (0.1 micromol/L), or isoproterenol (ISO, 10 mic

27 (TTX, 1 mumol/L), phentolamine (1 mumol/L), prazosin (0.1 mumol/L), or 6-hydroxydopamine (1 mmol/L)

28 ther with the alpha1-adrenoceptor antagonist prazosin (0.2 nmol) immediately after training in an inh

29 s in DNA and protein content were blocked by prazosin (0.3 micromol/L) and abolished in p47phox-/- ce

30 ther placebo or alpha1 -adrenergic blockade (prazosin; 0.05 mg kg( -1) ).

31 placebo or an alpha1-adrenoreceptor blocker (prazosin; 0.05 mg kg(-1)).

32 Pretreatment with prazosin (1 microgram/side) significantly diminished the

33 ed by the alpha(1)-adrenoreceptor antagonist prazosin (1 microM) and blocked by CPA(5 microM), an inh

34 of the alpha-adrenergic receptor antagonist prazosin (1.0 or 3.0 mg/kg) following nonreinforced cont

35 amine (30 microgram/5 microliter, icv, n=8), prazosin (10 microgram/5 microliter, icv, n=12) or alpha

36 repinephrine (10 mumol/L) in the presence of prazosin (10 mumol/L), an alpha 1-adrenergic blocker.

37 esence of an alpha(1)-adrenergic antagonist, prazosin (10(-6) m), selectively increases the PKA-depen

38 ns to NE (2 of 39 vessels) were inhibited by prazosin (10(-6) mol/L, an alpha1-receptor blocker).

39 in FA and 1A than did inhibiting alpha1 ARs (prazosin; 10(-8) m).

40 In the presence of atropine (1 microM) and prazosin (100 nM), pyridoxalphosphate-6-azophenyl-2',4'-

41 esence of the alpha1-adrenoceptor antagonist prazosin (100 nM), showing that NCTs can initiate local

42 microM), but not by nifedipine (1 microM) or prazosin (100 nM), suggesting that NCTs are generated by

43 inephrine (10 micromol/L) in the presence of prazosin (100 nmol/L) for 24 hours increased the number

44 the alpha1-, alpha2B- and alpha2C-antagonist prazosin (2 microM) were without effect.

45 de of alpha1-adrenoceptors by treatment with prazosin (3 mg/ kg, i.p.) 30 min prior to TBI produced e

46 alpha2-AR and beta-AR were assayed with [3H]prazosin, [3H]RX21002 and [125I]-iodo-pindolol autoradio

47 on in FBF in response to phenylephrine after prazosin (46 +/- 3 vs. 6 +/- 4 %; before vs. after block

48 15 nM), yohimbine (63 nM), ARC-239 (540 nM), prazosin (4900 nM), and terazosin (5000 nM) correlated b

49 spironolactone 25 mg/d, bisoprolol 10 mg/d, prazosin 5 mg/d, and rilmenidine 1 mg/d were sequentiall

50 d diabetic rats were treated with or without prazosin (5 mg.kg(-1).d(-1) for 3 wk).

51 zodioxane hydrochloride (WB-4101; 6.87), and prazosin (5.71).

52 of pretreatment with the alpha(1)-antagonist prazosin (.5 mg/kg) on MPH-induced improvement in sustai

53 mouse skeletal muscle: (1) administration of prazosin (50 mg l-1) thereby increasing blood flow; and

54 ent with the alpha 1-adrenoceptor antagonist prazosin (50 nmol/L) or removal of extracellular Ca2+ ab

55 ated by the alpha(1)-adrenoceptor antagonist prazosin (500 nM), indicating that it is not due to the

56 tudinal smooth muscle (compared with 8.6 for prazosin), 6.9 in anterior fibromuscular stroma (prazosi

57 ma (prazosin, 8.9), and 7.1 in bladder neck (prazosin, 8.5).

58 osin), 6.9 in anterior fibromuscular stroma (prazosin, 8.9), and 7.1 in bladder neck (prazosin, 8.5).

59 Prazosin, a potent and selective alpha1-adrenoceptor ant

60 This behavior was reversed by prazosin, a selective alpha(1)-AR inverse agonist, and m

61 The combination of prazosin, a selective alpha1-adrenergic antagonist, and

62 The selective alpha1-adrenoceptor antagonist prazosin abolished both the slowly developing contractio

63 Both i.v. hexamethonium and locally applied prazosin abolished the difference in FA tone and [Ca(2+)

64 Daily prazosin administration blunted but did not completely b

65 apillary to fibre ratio (C:F) in response to prazosin administration, along with the increases in lum

66 nist) and Rp-cAMPS (cAMP inhibitor), but not prazosin (alpha(1)-adrenoceptor antagonist), blocked CRF

67 20, but not with the alpha receptor blockers prazosin (alpha1) and/or yohimbine (alpha2).

68 5) constriction in 3A (inhibited by 10(-8) m prazosin; alpha1AR antagonist) while UK 14304 (UK; alpha

69 In partial agreement, the inverse agonist prazosin also caused a modest 20 +/- 2% increase in surf

70 Prazosin also decreased the EC50 for current activation

71 sponses to brachial artery administration of prazosin (an alpha(1)-adrenoceptor antagonist), yohimbin

72 nzamine could be mimicked by substitution of prazosin (an alpha1 antagonist, 4 mg/kg), but not idazox

73 ol, a beta 1-specific adrenergic antagonist, prazosin, an alpha 1-adrenergic antagonist, nor yohimbin

74 A second experiment examined whether prazosin, an alpha 1-adrenergic receptor antagonist, cou

75 .6 mumol/L, and this response was blocked by prazosin, an alpha 1-adrenergic receptor antagonist.

76 lating taste buds were reversibly blocked by prazosin, an alpha(1A) receptor antagonist.

77 her intravenous losartan (10 mg/kg b.wt) nor prazosin, an alpha1 adrenergic receptor antagonist, at d

78 Stimulation of Ip by NA was eliminated by prazosin, an alpha1-antagonist, but was unaffected by yo

79 Prazosin, an alpha1AR antagonist, attenuated LRA in Dbh+

80 re of alpha1- and beta-AR antagonists (1 muM prazosin and 10 muM propranolol).

81 Prazosin and betaxolol did not have a nonspecific reduci

82 Responses to NE were blocked by prazosin and depended on receptor density.

83 sms has led to the successful translation of prazosin and guanfacine for treating stress-related diso

84 Chronic nonresponders received nadolol+prazosin and had a third HVPG study.

85 vere trauma-related nightmares each received prazosin and placebo in a 20-week double-blind crossover

86 azine/isosorbide dinitrate was compared with prazosin and placebo therapy in V-HeFT I, and hydralazin

87 s were blocked by previous administration of prazosin and propranolol, and (3) vasopressin during CPR

88 s were blocked by previous administration of prazosin and propranolol, and 4) epinephrine in which bo

89 influenced by pre-incubation with atropine, prazosin and propranolol, but was reversed by TTX (1 mic

90 ts for alpha(1) and ss adrenergic receptors, prazosin and propranolol, respectively, indicated that b

91 At both pressures, the combination of prazosin and suramin virtually abolished constrictions.

92 over nonselective alpha1 antagonists such as prazosin and terazosin, with fewer side effects.

93 as well as the dissociation constant of (3)H-prazosin and the inhibition constant of CUMI-101.

94 (PE) and blocked by the alpha 1-antagonists prazosin and WB-4101, suggesting the presence of alpha 1

95 Adrenergic alpha1 antagonists prazosin and WB4101 and the nonselective alpha antagonis

96 L-arginine or the combination of prazosin and yohimbine alone did not affect the diameter

97 fos was blocked by a cocktail of an alpha1-(prazosin) and beta1-adrenoceptor (betaxolol) blocker but

98 e alpha(1)-adrenoceptor-selective antagonist prazosin, and are mimicked by the alpha(1)-adrenoceptor-

99 the efflux activity of mitoxantrone, BODIPY-prazosin, and Hoechst 33342, P485A exhibited a significa

100 the alpha(1)-adrenergic receptor antagonist, prazosin, and the alpha(2)-adrenergic receptor agonist,

101 iazide; 88%, 67%, and 40%, respectively, for prazosin; and 51%, 83%, and 100%, respectively, for capt

102 ked by the nonselective alpha1-AR antagonist prazosin as well as the selective alpha1D-AR antagonist

103 .g., mitoxantrone resensitization and BODIPY-prazosin assays).

104 ribed prazosin, only 18.2% were treated with prazosin at medical centers up to 499 miles (to convert

105 dose-dependent enhancement of retention, and prazosin attenuated the dose-response effects of clenbut

106 neuroepithelial cells retained specific 3[H]prazosin binding in culture.

107 eract with ABCG2 by a site distinct from the prazosin binding site as shown by their inability to dis

108 n of alpha1 receptors was detected using [3H]prazosin binding.

109 d were reflected in receptor proteins by [3H]prazosin binding.

110 bodipy-FL-vinblastine, calcein-AM, bodipy-FL-prazosin, bisantrene, and bodipy-FL-forskolin, but not f

111 rgic- and non-cholinergic-type MSDB neurons, prazosin blocked the effects of NA and PE mimicked the e

112 a in vitro; the alpha1, selective antagonist prazosin blocked this effect whereas chloroethylclonidin

113 decreased alpha1B-adrenoceptor density ([3H]prazosin Bmax) versus control groups by 12% (1 microM AO

114 hondrial translocation of p53 was blocked by prazosin, BMY 7378, apocynin, SB 202190, and pifithrin-a

115 de memantine, carbamazepine, citalopram, and prazosin, but none of these agents have sufficient evide

116 tiveness of methoxamine and nisoxetine while prazosin, by itself, had no effects on the seizure inten

117 the alpha 1 adrenergic selective antagonist prazosin compared to that of the alpha 2 adrenergic sele

118 (37%) immediately following exercise in the prazosin condition (t-test, P = 0.004, interaction effec

119 also were significantly more improved in the prazosin condition, and prazosin was well tolerated.

120 responses were inhibited by tetrodotoxin or prazosin, confirming the release of NA along perivascula

121 d that only preblocking with WAY-100635 plus prazosin decreased (11)C-CUMI-101 brain uptake to that o

122 However, concurrent infusion of prazosin did not alter the dose-response effects of 8-br

123 of the alpha1-adrenergic receptor antagonist prazosin did not cause any further change in sensitivity

124 Prazosin did not measurably displace [3H]CUMI-101 bindin

125 Prazosin differentially affected the binding of 5D3, a c

126 ese treatment effects differed from those of prazosin, diltiazem, or clonidine.

127 duced NE affinity (17) determined from [(3)H]prazosin displacement studies, whereas four mutations at

128 9-aminoacridines increase the rate of [(3)H]prazosin dissociation from the alpha1A- and alpha1B-adre

129 whereas patients on diltiazem, clonidine, or prazosin do not.

130 The authors' goal was to evaluate prazosin efficacy for nightmares, sleep disturbance, and

131 n alpha1AR activation should predict greater prazosin efficacy.

132 Prazosin (either 1 or 5 mg/kg b.wt., i.v.) was administe

133 alpha1-adrenoreceptor (alpha1AR) antagonist prazosin for combat posttraumatic stress disorder (PTSD)

134 ial of the alpha-1 adrenoreceptor antagonist prazosin for combat trauma nightmares, sleep quality, gl

135 These data support the efficacy of prazosin for nightmares, sleep disturbance, and other PT

136 tment of ADHD and related PFC disorders, and prazosin for the treatment of PTSD.

137 oup ranged from 70% for clonidine to 90% for prazosin for younger black men, from 50% for captopril t

138 he dissociation rate of the antagonist [(3)H]prazosin from the alpha(1A)-adrenergic receptor in a con

139 23, doxorubicin, mitoxantrone, and BODIPY-FL-prazosin) from MCF-7/DX1 cells.

140 After cocaine place conditioning, prazosin had no effect on the rate of extinction over 8

141 While mecamylamine and prazosin had no effect, scopolamine, methysergide and MD

142 ctiveness of the alpha(1)-adrenergic blocker prazosin hydrochloride in the treatment of nightmares an

143 The antihypertension agent iodoazidoaryl prazosin (IAAP) has been made using a convergent route i

144 f 21 at alpha(1)-adrenergic receptors ([(3)H]prazosin, IC(50) = 0.54 microM) and dopamine D2 receptor

145 lonidine, diltiazem, hydrochlorothiazide, or prazosin in a double-masked trial.

146 lonidine, diltiazem, hydrochlorothiazide, or prazosin in a double-masked trial.

147 In contrast, the dissociation data for [(3)H]prazosin in the presence of the amiloride analogs were n

148 In 10 subjects, prazosin increased FBF from 2.4 +/- 0.3 to 5.8 +/- 1.0 m

149 ephrine plus an alpha(1)-adrenergic blocker, prazosin, increased the amplitude of SR Ca(2+) release f

150 fic alpha(1)-adrenergic receptor antagonist, prazosin, inhibited the stimulatory effects of NE by app

151 We found that the antihypertensive drug Prazosin inhibits endocytic sorting by an off-target per

152 s significantly less than at 2 days, whereas prazosin-insensitive muscarinic contraction was increase

153 icating the possible involvement of alpha2A (prazosin-insensitive) and non-alpha2A (prazosin-sensitiv

154 Prazosin is a centrally active alpha(1) adrenergic antag

155 Prazosin is a powerful tool for rapid and reversible per

156 Prazosin is also a potent cytokinesis inhibitor, likely

157 Prazosin is effective for combat-related PTSD with traum

158 phrine and an alpha(1)-adrenergic antagonist prazosin is not restored by pertussis toxin treatment de

159 swell)) by noradrenaline; in the presence of prazosin, KT5720 blocked the inhibitory action of noradr

160 sin, a photoaffinity analog of the substrate prazosin, labels multiple variants of ABCG2 specifically

161 Prazosin (mean dose=9.5 mg/day at bedtime, SD=0.5) was s

162 ence of the alpha(1)-adrenoceptor antagonist prazosin, noradrenaline reduced I(Cl(swell).) The phosph

163 beta(1)-AR stimulation (norepinephrine plus prazosin) of I(Ca,L) was not altered.

164 ects of the alpha(1)-adrenoceptor antagonist prazosin on lordosis behavior in E(2)- and P-treated fem

165 evaluating alpha(1)-adrenoceptor antagonist prazosin on NBF, MNC, as well as metabolic imbalances an

166 Tacoma, Washington, in 2004 were prescribed prazosin, only 18.2% were treated with prazosin at medic

167 fected by the alpha1 adrenoceptor antagonist prazosin or by capsaicin (which inhibits the function of

168 ers were randomly assigned to treatment with prazosin or placebo for 15 weeks.

169 In contrast, either prazosin or WB4101 partially reversed the increase in th

170 he selective alpha1-adrenoceptor antagonists prazosin or WB4101 potentiated the increase in the foot-

171 tored with inhibition of alpha1- (0.1 microM prazosin) or alpha2- (0.1 microM RX821002) adrenorecepto

172 ll invasion could not be inhibited by alpha (prazosin)- or beta (propanolol)-adrenergic blockers or L

173 of alpha1-adrenoceptors for norepinephrine, prazosin, or subtype-selective antagonists, suggesting t

174 Phentolamine, prazosin, or tetrodotoxin (1 microM) during muscle stret

175 sence of the alpha1 adrenoceptor antagonist, prazosin, or the MAP kinase kinase (MEK) inhibitor, U012

176 level and high altitude (placebo P = 0.287; prazosin: P = 0.110); (2) FMD remained unchanged after m

177 Prazosin participants (n = 32) and placebo participants

178 In prazosin participants, each 10-mm Hg higher baseline sta

179 p-chlorophenylalanine (serotonin depletor), prazosin (PRAZ, selective alpha1-receptor antagonist), W

180 Regardless of the prazosin pre-treatment, plasma LH concentrations showed

181 tested, the prototypical alpha1-antagonist, prazosin produced a variable degree of block (9-58%), fu

182 depleted diets, mice fed the same diets with prazosin (PRZ, an alpha-1 adrenoceptor antagonist) or 6-

183 culture of the alpha1-adrenergic antagonist prazosin (Pz) at 10(-7) M.

184 s were reduced (15-35 mmHg) with individual (prazosin, rauwolscine) or combined (phentolamine) alpha-

185 ehicle-treated mice did not, suggesting that prazosin reduced the persistent effects of extinction (E

186 he purinergic component of vasoconstriction (prazosin-resistant) was almost abolished by the L-type C

187 Pre-treatment with prazosin reversed the HS-induced pressor response to a h

188 mg of placebo (SD=0.8) for men and 1.7 mg of prazosin (SD=0.5) and 2.0 mg of placebo (SD=0.0) mg for

189 ean achieved midmorning doses were 4.0 mg of prazosin (SD=1.4) and 4.8 mg of placebo (SD=0.8) for men

190 mg of placebo (SD=3.3) for men and 7.0 mg of prazosin (SD=3.5) and 10.0 mg of placebo (SD=0.0) for wo

191 Mean achieved bedtime doses were 15.6 mg of prazosin (SD=6.0) and 18.8 mg of placebo (SD=3.3) for me

192 that responded directly to NA and PE with a prazosin-sensitive inward current were found within the

193 ha2A (prazosin-insensitive) and non-alpha2A (prazosin-sensitive) receptors.

194 Prazosin stabilizes a normally transient interaction bet

195 il, nicardipine, tetraphenylphosphonium, and prazosin, stimulated ATPase activities of both the wild-

196 rane preparations, neither the basal nor the prazosin-stimulated ( approximately 2-fold) ATPase activ

197 cyclosporin A had no effect on the basal or prazosin-stimulated ATPase activity of ABCG2, whereas bo

198 r ABCG2 localization, transport activity, or prazosin-stimulated ATPase activity.

199 t 97% less likely in 2004 to be treated with prazosin than patients within Puget Sound.

200 out 63% less likely in 2004 to be prescribed prazosin than their counterparts treated within Puget So

201 oxamine, the alpha 1-adrenoceptor antagonist prazosin, the alpha 2-adrenoceptor antagonists idazoxan

202 During 3 min of EFS in prazosin, the frequency of jCaTs declined markedly; at s

203 oup of four subjects, increasing the dose of prazosin threefold did not evoke further forearm vasodil

204 Binding of the antagonist prazosin to Y348A receptors was similar to that of wild-

205 ever, the ability of Pgp substrates (such as prazosin) to stimulate ATP hydrolysis and facilitate van

206 ne + rauwolscine) or alpha 2-AR (UK 14,304 + prazosin) tone was induced in rat cremaster skeletal mus

207 red mitoxantrone, pheophorbide a, and BODIPY-prazosin transport, particularly in the double leucine m

208 wing postextinction reconditioning, however, prazosin-treated mice showed a robust place preference,

209 alpha1AR activation in PTSD is the target of prazosin treatment action, higher brain alpha1AR activat

210 Subsequent experiments under prazosin treatment established the apoptosis dose-respon

211 Prazosin was effective for trauma nightmares, sleep qual

212 a second experiment, an alpha-1 antagonist, prazosin was given with phenylephrine to block the presu

213 However, prazosin was unable to prevent internalization of antibo

214 (3)H-prazosin was used to determine the maximum number of bin

215 Prazosin was well tolerated, and blood pressure changes

216 more improved in the prazosin condition, and prazosin was well tolerated.

217 endent manner by the competitive antagonists prazosin, WB4101, and 5-methylurapidil, with IC50 values

218 f affinity (4-1200-fold) for the antagonists prazosin, WB4101, BMY7378, (+) niguldipine, and 5-methyl

219 azosin ([125I]IAAP), a photoactive analog of prazosin, we have demonstrated the presence of two nonid

220 Hydrochlorothiazide and prazosin were best in low- and medium-renin profiles; ca

221 vels of the alpha1-selective radioligand 3[H]prazosin were detected in the forebrain of the rat embry

222 blocked by the alpha1-adrenergic antagonist prazosin, whereas signaling in the NPE but not PE was bl

223 After treatment with prazosin, which exhibits inverse agonist properties, the

224 dual symptoms suggest that studies combining prazosin with effective psychotherapies might demonstrat

225 ergic signaling with the receptor antagonist prazosin worsens sorafenib-induced cardiomyopathy in zeb

226 ergic drugs tested in these two brain areas; prazosin, yohimbine, amphetamine, SKF 38393 and SCH 2339