ライフサイエンスコーパス: prazosin

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

2 raction to EFS in the absence of suramin and prazosin.

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

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

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

6 controls, and this decrease was prevented by prazosin.

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

8 rats, and this reduction was ameliorated by prazosin.

9 h hydrochlorothiazide than with captopril or prazosin.

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

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

12 cells with the alpha1-adrenergic antagonist prazosin.

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

14 effect was abolished by propranolol but not prazosin.

15 affected by the alpha1-adrenergic antagonist prazosin.

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

17 blocked by the alpha 1-adrenergic antagonist prazosin.

18 alol, and the alpha1-adrenoceptor antagonist prazosin.

19 oxantrone or the fluorescent compound BODIPY-prazosin.

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

21 having PTSD who received a prescription for prazosin.

22 ir ability to efflux mitoxantrone and BODIPY-prazosin.

23 in the presence of 140 mum suramin and 1 mum prazosin.

24 1 adrenergic receptor (alpha1-AR) antagonist prazosin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 omized, controlled proof-of-concept trial of prazosin (16 mg/day, with a 2-week titration) was conduc

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

49 erved changes following discontinuation (eg, prazosin); 2) attenuation or loss of on-treatment effect

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

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

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

53 15 nM), yohimbine (63 nM), ARC-239 (540 nM), prazosin (4900 nM), and terazosin (5000 nM) correlated b

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

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

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

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

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

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

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

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

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

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

64 Prazosin, a potent and selective alpha1-adrenoceptor ant

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

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

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

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

69 During acute inflammation, prazosin abrogated exercise-enhanced neutrophil clearanc

70 Daily prazosin administration blunted but did not completely b

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

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

73 20, but not with the alpha receptor blockers prazosin (alpha1) and/or yohimbine (alpha2).

74 ol (beta-adrenergic receptor antagonist) and prazosin (alpha1-adrenergic receptor antagonist) reduced

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

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

77 Prazosin also decreased the EC50 for current activation

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

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

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

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

82 .6 mumol/L, and this response was blocked by prazosin, an alpha 1-adrenergic receptor antagonist.

83 Prazosin, an alpha(1) receptor antagonist, reduced moder

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

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

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

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

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

89 Prazosin and betaxolol did not have a nonspecific reduci

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 drenergic receptor antagonists (propranolol, prazosin, and atipamezole: PPA), enhanced glymphatic flo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 als with high alcohol withdrawal symptoms on prazosin compared with placebo also showed significantly

128 (37%) immediately following exercise in the prazosin condition (t-test, P = 0.004, interaction effec

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

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

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

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

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

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

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

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

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

138 9-aminoacridines increase the rate of [(3)H]prazosin dissociation from the alpha1A- and alpha1B-adre

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

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

141 n alpha1AR activation should predict greater prazosin efficacy.

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

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

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

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

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

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

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

149 23, doxorubicin, mitoxantrone, and BODIPY-FL-prazosin) from MCF-7/DX1 cells.

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

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

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

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

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

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

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

157 withdrawal symptoms moderate the efficacy of prazosin in reducing alcohol intake and associated secon

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

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

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

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

162 In contrast, prazosin inhibition of alpha-1 NERs systemically reduced

163 Finally, prazosin inhibition of CLAD and AOD was not correlated w

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

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

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

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

168 Prazosin is a powerful tool for rapid and reversible per

169 Prazosin is also a potent cytokinesis inhibitor, likely

170 Prazosin is effective for combat-related PTSD with traum

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

172 SMD = -0.45; -0.85 to -0.05; p = 0.085) and prazosin (k = 3; n = 110; SMD = -0.52; -1.03 to -0.02; p

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

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

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

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

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

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

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

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

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

182 Lower blood pressure was observed either in prazosin or losartan-treated adult or aged SHRs.

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

184 of intrinsic nerves, which were inhibited by prazosin or the Na(V)1 blocker tetrodotoxin.

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

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

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

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

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

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

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

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

193 Prazosin participants (n = 32) and placebo participants

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

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

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

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

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

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

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

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

202 nts with high alcohol withdrawal symptoms on prazosin reported 7.07% heavy drinking days and 27.46% d

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

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

205 drawal symptoms as a prognostic indicator of prazosin's efficacy in the treatment of AUD.

206 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

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

208 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

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

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

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

212 Prazosin stabilizes a normally transient interaction bet

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 Prazosin treatment alleviated the effects of hypertensio

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

230 awal symptoms are a significant moderator of prazosin treatment response for alcohol use outcomes and

231 Prazosin was effective for trauma nightmares, sleep qual

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

233 No such benefit of prazosin was observed in those reporting low or no alcoh

234 However, prazosin was unable to prevent internalization of antibo

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

236 Prazosin was well tolerated, and blood pressure changes

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

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

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

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

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

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

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

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

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

246 the solubility of the antihypertensive drug prazosin without affecting its biological profile.

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

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