ライフサイエンスコーパス: phenylephrine

1 hrine, EPI), and metabolic degradation (C-11 phenylephrine).

2 ertension (160-170mm Hg, group 2, n=6) using phenylephrine.

3 r influence on cortical oxygenation than did phenylephrine.

4 ure was manipulated with the vasoconstrictor phenylephrine.

5 reduced renal oxygen delivery more than did phenylephrine.

6 d constriction, respectively, in response to phenylephrine.

7 the alpha(1)-adrenoceptor-selective agonist phenylephrine.

8 changed by fluid percussion brain injury and phenylephrine.

9 s infusion of sodium nitroprusside (SNP) and phenylephrine.

10 and nuclei, and back, during 2 h exposure to phenylephrine.

11 pes, consistent with blunted constriction to phenylephrine.

12 es with hypertrophy induced by 10 micromol/L phenylephrine.

13 ation at Ser695 in the fiber pretreated with phenylephrine.

14 rdiomyocytes stimulated by angiotensin II or phenylephrine.

15 lost following alpha(1a)AR stimulation with phenylephrine.

16 >6-fluoronorepinephrine > norepinephrine >>> phenylephrine.

17 induced increased cell size was inhibited by phenylephrine.

18 than those induced by equi-pressor doses of phenylephrine.

19 heart rate responses to increasing doses of phenylephrine.

20 in BP and HR after topical administration of phenylephrine.

21 nly administered alternative vasopressor was phenylephrine.

22 uction and attenuated hypertrophy to Iso and phenylephrine.

23 vasoconstrictor effect of norepinephrine and phenylephrine.

24 jury in untreated, preinjury, and postinjury phenylephrine (1 microg/kg/min intravenously) treated ma

25 xybuprocain 0.4%, cocain 4%, tropicamide 1%, phenylephrine 10%, diclophenac 0.1% along with chloramph

26 cription was increased by hypoxia but not by phenylephrine (10 microM), angiotensin II (100 nM), or i

27 o mydriatic eye drops (tropicamide [1%] plus phenylephrine [10%]).

28 at 20 to 30 minutes following application of phenylephrine, 10%, and HR decreased by 60 minutes or lo

29 r HR, and the changes in BP and HR seen with phenylephrine, 10%, are short lived.

30 Following application of phenylephrine, 10%, BP increased at 5 and 10 minutes (me

31 (100 nmol/L), endothelin-1- (10 nmol/L), or phenylephrine- (10 micromol/L) induced hypertrophic cult

32 In young mice, stimulating alpha1 ARs (phenylephrine; 10(-7) m) and alpha2 ARs (UK 14304; 10(-7

33 Phenylephrine (100 mumol/L), an alpha1 adrenergic agonis

34 ne (-30 +/- 2 versus -36 +/- 7%; P = 0.4) or phenylephrine (-16 +/- 2 versus -19 +/- 3%; P = 0.3) in

35 Data were available for phenylephrine, 2.5%, at 20 to 30 minutes and 60 minutes

36 Thus, phenylephrine, 2.5%, is safe to use in clinical routine.

37 Phenylephrine, 2.5%, leads to no clinically relevant cha

38 After continuous infusion of phenylephrine (20 mg/kg per day) for 14 days, wild-type

39 s to tyramine (-30 +/- 3 versus -41 +/- 3%), phenylephrine (-25 +/- 4 versus -45 +/- 5%), and dexmede

40 igation and puncture, vascular reactivity to phenylephrine (3 and 30 nmol/kg) before and after 7-nitr

41 ctive ingredients: tropicamide (0.25 mg) and phenylephrine (5.38 mg).

42 , and it can be rescued by administration of phenylephrine, a catecholamine that raises vessel tone.

43 hat acute treatment of cardiac myocytes with phenylephrine, a prohypertrophic stimulant, transiently

44 d pressor responses and vasoconstrictions to phenylephrine, accompanied by enhanced membrane depolari

45 Vascular response to phenylephrine, acetylcholine, and sodium nitroprusside i

46 Effective prophylactic phenylephrine administration can be associated with redu

47 example, cardiac hypertrophy in response to phenylephrine agonist infusion for 2 wk was largely blun

48 uctance (FVC) to intra-arterial infusions of phenylephrine (alpha(1)-agonist) and dexmedetomidine (al

49 sponses to local intra-arterial infusions of phenylephrine (alpha(1)-agonist) and dexmedetomidine (al

50 e (evokes endogenous noradrenaline release), phenylephrine (alpha1-agonist) and clonidine (alpha2-ago

51 yramine (evokes noradrenaline (NA) release), phenylephrine (alpha1-agonist) and dexmedetomidine (alph

52 Phenylephrine (an alpha1AR agonist) potency was greater

53 s the role and mechanisms of action by which phenylephrine, an alpha(1) -adrenergic agonist stimulati

54 First, preadipocytes were treated with phenylephrine, an alpha-adrenergic receptor agonist, to

55 After pupil dilation with 2.5% phenylephrine and 1% tropicamide, ocular alignment was r

56 ced pharmaceutically by the addition of 2.5% phenylephrine and 1% tropicamide.

57 system, and concentration-response curves to phenylephrine and acetylcholine were evaluated.

58 ithdrew beta-blockers and diuretics and used phenylephrine and albumin infusion to evaluate the respo

59 erve activity, and pressor responsiveness to phenylephrine and angiotensin II during hypotensive seps

60 and restored pressor responsiveness to both phenylephrine and angiotensin II toward preseptic levels

61 Pressor responses to increasing doses of phenylephrine and angiotensin II were measured at baseli

62 ivity, restored vascular sensitivity to both phenylephrine and angiotensin II, and resulted in better

63 ity (~70%), and blunted pressor responses to phenylephrine and angiotensin II.

64 The increase in [Ca(2+)](i) caused by phenylephrine and BzATP used simultaneously or sequentia

65 support 3 previously reported associations: phenylephrine and endocardial cushion defect (odds ratio

66 citrulline reverts the hyporesponsiveness to phenylephrine and increases the vasoconstrictor effect o

67 The protein secretion in response to phenylephrine and isoproterenol showed that direct stimu

68 phy induced by hypertrophic agonists such as phenylephrine and leukemia inhibitory factor.

69 f uni-x sheep had enhanced responsiveness to phenylephrine and nitrotyrosine staining and reduced sen

70 mediating cardiac hypertrophy in response to phenylephrine and pressure overload.

71 on, vasoconstriction after exposure to 1 muM phenylephrine and released nitric oxide in a manner simi

72 Vasoconstrictor responses to phenylephrine and serotonin challenge in the thoracic ao

73 Data were synthesized by concentration of phenylephrine and time of measurement following topical

74 ated cardiomyocyte hypertrophic responses to phenylephrine and to chronic pressure overload, but it a

75 during steady-state stimulus conditions (pre-phenylephrine), and after 2 min of phenylephrine (PE; an

76 an [SE], 134.2% [5.2%] vs 100.9% [2.9%], for phenylephrine, and 156.0% [5.6%] vs 125.1% [7.5%], for s

77 ation, as well as activation with carbachol, phenylephrine, and KCl, were lower in old than in young

78 blood pressure was maintained by infusion of phenylephrine, and we also measured the effects of trans

79 High tidal volume ventilation impaired phenylephrine- and acetylcholine-induced responses in pu

80 MAPK activation while completely inhibiting phenylephrine- and EGF-stimulated MAPK activation.

81 carbachol-stimulated MAPK with no effect on phenylephrine- and EGF-stimulated MAPK activation.

82 RGS2 knockdown increased phenylephrine- and endothelin-1-induced phospholipase Cb

83 We investigated the role of pannexins in phenylephrine- and KCl-mediated constriction of resistan

84 and [Ca(2+)]i in response to locally applied phenylephrine, Ang II, arginine vasopressin, elevated [K

85 wing transverse aortic constriction (TAC) or phenylephrine/Ang II infusion, but showed no reduction i

86 tropic responses to exogenous bolus doses of phenylephrine, angiotensin II and arginine vasopressin w

87 Fetal treatment with phenylephrine, angiotensin II and vasopressin produced s

88 and tonic contractile responses elicited by phenylephrine, angiotensin II, endothelin-1, U46619, and

89 Abs did not alter the vascular reactivity to phenylephrine, angiotensin II, or acetylcholine in nativ

90 , stimulation of the alpha1aAR with low dose phenylephrine ( approximately 10(-8) M) induced an Erk-d

91 asurements were obtained by concentration of phenylephrine as a mean change and its standard deviatio

92 eduction in force development in response to phenylephrine as well as sensitizing the muscle to acety

93 and in vivo and ex vivo arterial response to phenylephrine at 18 hours after induction of murine endo

94 the time following administration of topical phenylephrine at which measurements were obtained by con

95 006) and was related to the SBP responses to phenylephrine before GB (R2=0.71, P<0.0001).

96 Phenylephrine blunted extracellular signal-related kinas

97 growth in response to the alpha1-AR agonist phenylephrine but not to the beta-AR agonist isoproteren

98 hr-696 and Thr-853 were also stimulated with phenylephrine but significantly less than in bladder tis

99 te signals for some small molecules, such as phenylephrine, by up to 3-fold.

100 We used photolysis of caged phenylephrine, caged guanosine 5'-O-(thiotriphosphate) (

101 ylephrine-induced protein secretion, whereas phenylephrine caused a 2.2-fold increase in cGMP.

102 that alpha-adrenergic receptor activation by phenylephrine causes a transient, PKD-dependent HDAC5-GF

103 suppressed 8-pCPT-AM-mediated relaxation in phenylephrine-contracted arteries (24.8 +/- 4.9% relaxat

104 T-AM) elicited a 77.6 +/- 7.1% relaxation of phenylephrine-contracted arteries over a 5 min period (m

105 In contrast, phenylephrine contractions (alpha(1) agonist) were enhan

106 ined unchanged during time and hypertensive (phenylephrine) control experiments.

107 vasopressin/selepressin, angiotensin II, and phenylephrine could have a fundamental advantage over no

108 Phenylephrine decreased impairment of hypotensive pial a

109 table, acetylcholine-dependent relaxation or phenylephrine-dependent constriction in aortic rings iso

110 Equi-pressor infusion of phenylephrine did not significantly reduce RBF or renal

111 n of the systolic BP [SBP] response to bolus phenylephrine during versus before GB) than men, 51 heal

112 rfusion pressure of 70 mm Hg with the use of phenylephrine early after injury in the immature brain w

113 ed pressor responses, because bolus doses of phenylephrine evoked attenuated pressor responses after

114 ) medium, the alpha(1)-adrenoceptor agonist, phenylephrine evoked bursts that were highly similar to

115 Arginine vasopressin was as effective as phenylephrine for maintaining cerebral perfusion pressur

116 hat arginine vasopressin was as effective as phenylephrine for maintaining tissue oxygenation during

117 pupil dilation with 1 % tropicamide and 10 % phenylephrine for retinal examination, acute elevation o

118 ely and under natural viewing conditions and phenylephrine (for accommodative efforts ranging from 0

119 Stimulation of the alpha1aAR by high dose phenylephrine (>10(-7) M) induces an antiproliferative,

120 P14 activity is increased by angiotensin II, phenylephrine, GTP, and guanosine 5'-O-[gamma-thio]triph

121 The selective alpha1 adrenergic agonist phenylephrine had no effect on membrane potential but di

122 Phenylephrine has been used safely in mothers with cardi

123 Topical phenylephrine hydrochloride is routinely administered wi

124 ate to a change in blood pressure induced by phenylephrine i.v. was significantly increased (610+/-17

125 ential bolus injections of nitroprusside and phenylephrine in 14 young healthy subjects.

126 bolus injections of sodium nitroprusside and phenylephrine in 22 young, 21 older sedentary and 10 old

127 thoracic aorta segments were stimulated with phenylephrine in the presence or absence of 7-nitroindaz

128 rogates the cardiomyocyte growth response to phenylephrine in vitro through inhibition of p38 and the

129 Phenylephrine increased ATP release from pieces in a tim

130 Phenylephrine increased BP by 11, 23 and 37% from baseli

131 atively, increased IP3 production induced by phenylephrine increased Ca(2+) transient and wave freque

132 based RBCK1 overexpression in the absence of phenylephrine increased cardiac cell size.

133 Phenylephrine increased NO production in a time- and con

134 s in target phosphorylation at CaMKII sites: phenylephrine increases histone deacetylase 5 phosphoryl

135 Phenylephrine induced a dose-dependent contraction of WT

136 ownregulation of PDE1A using siRNA prevented phenylephrine induced pathological myocyte hypertrophy a

137 Following chronic hypoxia during pregnancy, phenylephrine induced significantly higher pressor respo

138 In primary cultured rat cardiomyocytes, phenylephrine-induced activation of nuclear factor-kappa

139 Phenylephrine-induced aortic contraction was reduced in

140 Baroreflex heart rate responses to phenylephrine-induced blood pressure elevation and IKACh

141 (CXCL12, ubiquitin) reduced the EC50 of the phenylephrine-induced blood pressure response three- to

142 heteromeric complexes in VSMC and abolished phenylephrine-induced Ca(2+) fluxes and MLC2 phosphoryla

143 PKC down-regulation attenuates phenylephrine-induced Ca(2+) wave velocity, whereas resp

144 In phenylephrine-induced cardiac hypertrophy, ang1-256 redu

145 ing postnatal development and decreased with phenylephrine-induced cardiac hypertrophy, whereas tie2

146 emodeling and overexpressed ang1 monomers in phenylephrine-induced cardiac hypertrophy.

147 For example, both AC6 and AC6mut reduced phenylephrine-induced cardiac myocyte hypertrophy and ap

148 -33 markedly antagonized angiotensin II- and phenylephrine-induced cardiomyocyte hypertrophy.

149 reduced the ability of 8-pCPT-AM to reverse phenylephrine-induced contraction (arteries relaxed by o

150 Phenylephrine-induced contraction and nitric oxide donor

151 and late sustained phases, respectively, of phenylephrine-induced contraction, regardless of arteria

152 ic, U46619, and had no significant action on phenylephrine-induced contractions.

153 Functionally, phenylephrine-induced heterocellular calcium communicati

154 y RNA interference technology attenuated the phenylephrine-induced hypertrophic response in cardiomyo

155 ell death, whereas Yap1 depletion attenuated phenylephrine-induced hypertrophy and augmented apoptosi

156 show that in vitro, GHRH(1-44)NH2 attenuates phenylephrine-induced hypertrophy in H9c2 cardiac cells,

157 tes compared with nonsilencing controls in a phenylephrine-induced hypertrophy model.

158 ocytes significantly inhibited and increased phenylephrine-induced hypertrophy, respectively.

159 tl1 promoted AMPK activation and antagonized phenylephrine-induced hypertrophy.

160 dogenous RBCK1 protein levels increased upon phenylephrine-induced hypertrophy.

161 ct ARVM, the ability of CPA to attenuate the phenylephrine-induced increase in NHE1 phosphorylation a

162 e corroborated in vivo, where acute systemic phenylephrine-induced increases in blood pressure evoked

163 istically, beta3-AR overexpression inhibited phenylephrine-induced nuclear factor of activated T-cell

164 )(-) production in the nucleus and prevented phenylephrine-induced oxidation and nuclear exit of HDAC

165 NF-kappaB, it inhibited angiotensin II- and phenylephrine-induced phosphorylation of inhibitor of NF

166 We observed an inhibition of phenylephrine-induced proliferation in small cholangiocy

167 th oxadiazoloquinoxalin (ODQ) also inhibited phenylephrine-induced protein secretion, whereas phenyle

168 Furthermore, PDE1A plays a critical role in phenylephrine-induced reduction of intracellular cGMP- a

169 line-mediated vascular relaxation as well as phenylephrine-induced vasoconstriction.

170 -activated K(+) (BKCa) channels in buffering phenylephrine-induced vasoconstrictions was decreased, w

171 BP was increased stepwise with phenylephrine infusion at 0.5, 1.0 and 2.0 microg kg(-1)

172 Prophylactic phenylephrine infusion can cause hypertension if increas

173 y and related gene expression due to chronic phenylephrine infusion.

174 ertrophy following 2 weeks of angiotensin II/phenylephrine infusion.

175 uring SNP, and increased by 21 +/- 8% during phenylephrine infusion.

176 more exuberant growth in response to chronic phenylephrine infusion.

177 blunted mean arterial pressure responses to phenylephrine injection (55+/-10% versus 93+/-7%, P<0.05

178 Intracameral phenylephrine is a highly efficient measure for prophyla

179 Phenylephrine is often used for management of cerebral p

180 Phenylephrine is the current vasopressor of choice for t

181 s the results based on endothelin-1, because phenylephrine is thought to act exclusively through Galp

182 ric oxide, sildenafil, dopamine, dobutamine, phenylephrine, isoproterenol, and vasopressin.

183 Phenylephrine, L-NMMA or placebo was administered on dif

184 but attenuated alpha1-adrenoreceptor agonist phenylephrine-mediated inhibition (40 microM; NORM, 36 +

185 endent mechanism, whereas isoproterenol- and phenylephrine-mediated mechanisms had a significant auto

186 h increased 20-HETE-dependent sensitivity to phenylephrine-mediated vasoconstriction and with decreas

187 Sequential nitroprusside and phenylephrine (modified Oxford test) were used to evalua

188 Neither phenylephrine nor placebo altered basal choroidal blood

189 For 120-480 mins, phenylephrine, normal saline, and dextrose were administ

190 Stimulation of myocytes with phenylephrine or angiotensinII causes GRK5 to leave the

191 After 120 mins, phenylephrine or arginine vasopressin was titrated to ce

192 Stimulation of alpha1A-AR with phenylephrine or direct activation of PKC with phorbol e

193 Stimulation of IP3 production by phenylephrine or endothelin-1 had a positive chronotropi

194 ll hypertrophy induced by the alpha-agonists phenylephrine or endothelin-1 was inhibited by MDM2 over

195 Intracameral phenylephrine or epinephrine, either by direct injection

196 nstriction (without altering the response to phenylephrine or KCl) and preventing O2-induced increase

197 easured while AP was altered by infusions of phenylephrine or nitroprusside (+/-60 mmHg over 60-90 s)

198 in cultured neonatal rat cardiomyocytes with phenylephrine or overexpression of a constitutively acti

199 culated from the rise in pressure induced by phenylephrine or the fall in pressure evoked by sodium n

200 sized that either the alpha-receptor agonist phenylephrine or the nitric oxide synthase (NOS) inhibit

201 ontractions to the alpha1-adrenergic agonist phenylephrine or the thromboxane (TX) A2 analog U-46619

202 carbachol, the alpha(1D)-adrenergic agonist phenylephrine, or EGF.

203 s or of either the partial alpha(1)-agonist, phenylephrine, or full alpha(2)-agonist, dexmedetomidine

204 ressure and was responsive to treatment with phenylephrine (PE) (10(-5) m) and ACh (10(-5) m).

205 Similarly, arteriolar constriction with phenylephrine (PE) (10(-5) m) induced a significant incr

206 rtas from these mice were hypocontractile to phenylephrine (PE) and had increased basal NO generation

207 as stimulated with increasing bolus doses of phenylephrine (PE) following maternal vehicle or allopur

208 by 5 min) of the alpha(1)-adrenergic agonist phenylephrine (PE) in combination with 8-Br-cGMP yielded

209 nergic stimulation of H9c2 cardiomyocytes by phenylephrine (PE) increased the cell size with enhanced

210 The alpha-adrenergic agonist phenylephrine (PE) increased tissue stress and stiffness

211 y, treatment of rat mesenteric arteries with phenylephrine (PE) led to the increase in CAS tyrosine p

212 renergic receptor (alpha1-AR) stimulation by phenylephrine (PE) on L-type Ca2+ current (I(Ca,L)) in c

213 ded in dorsal finger during iontophoresis of phenylephrine (PE) or clonidine (0.5 mm, seven 0.1 mA pu

214 In isolated mesenteric arterial rings, phenylephrine (PE) produced concentration-dependent vaso

215 w microneedle (HM) was prepared to deliver a phenylephrine (PE) solution into the anal sphincter musc

216 lamines norepinephrine (NE), epinephrine, or phenylephrine (PE) than are the alpha1B and alpha1D subt

217 ated that stimulation of cardiomyocytes with phenylephrine (PE), a well known hypertrophic agonist, s

218 administration of alpha-adrenergic agonists (phenylephrine (PE), alpha(1); clonidine (CL), alpha(2)).

219 phic stimuli, including isoproterenol (ISO), phenylephrine (PE), and endothelin-1 (ET-1).

220 metabolic inhibition than an alpha1-agonist, phenylephrine (PE), in the exercising human thigh.

221 I (Ang II) and the alpha-adrenergic agonist, phenylephrine (PE), on cardiac energy metabolism in expe

222 t induce hypertrophy, endothelin-1 (ET1) and phenylephrine (PE), trigger comparable global PKD activa

223 ith a dose-response using the alpha1-agonist phenylephrine (PE), with and without the nitric oxide sy

224 During phenylephrine (PE)-induced contraction, SNP reduced CPI-

225 omyocytes, overexpression of miR-378 blocked phenylephrine (PE)-stimulated Ras activity and also prev

226 tricle of aorta-constricted rats in vivo and phenylephrine (PE)-treated myocytes in vitro.

227 Phenylephrine (PE)-triggered hypertrophy and autophagy i

228 infusion of an alpha-adrenoreceptor agonist, phenylephrine (PE, 0.025 to 0.8 mug kg min) and an alpha

229 ed the responses to IGF1 (10 nmol/liter) and phenylephrine (PE, 20 mumol/liter), a known GATA4 activa

230 10(9)-1 x 10(4)m), constrictor responses to phenylephrine (PE; 1 x 10(9)-1 x 10(4)m), and flow-induc

231 Contractile response to phenylephrine (PE; 10(-10) to 10(-4)M), an alpha1-adrene

232 atheter) to local intra-arterial infusion of phenylephrine (PE; alpha1 -adrenoceptor agonist) were ca

233 ductance (FVC) to intra-arterial infusion of phenylephrine (PE; alpha1 -agonist) during ATP or contro

234 Phenylephrine (PE; alpha1AR agonist) evoked greater (P <

235 ions (pre-phenylephrine), and after 2 min of phenylephrine (PE; an alpha1 -adrenoceptor agonist) infu

236 d by stepwise sodium nitroprusside (SNP) and phenylephrine (PhE) infusion.

237 le function develops in response to low dose phenylephrine (PHE, 100 nM) in controls, while function

238 ed with either an alpha1-adrenergic agonist, phenylephrine (PHE; 0.5 mg/kg BW), an alpha2-adrenergic

239 es, bath application of the alpha(1)-agonist phenylephrine (PHE; 10 microM) depolarized 10 of 25 neur

240 take and no washout in healthy humans; (11)C-phenylephrine (PHEN), a tracer of vesicular leakage and

241 were greater in males, which were blunted by phenylephrine pre- or postfluid percussion brain injury.

242 ne exerted a potent vasodilatatory effect on phenylephrine pre-constricted arterial rings, which was

243 acological AMPK activation by A769662 caused phenylephrine pre-constricted UtA from normoxic or hypox

244 Measurements were obtained under phenylephrine preoperatively and under natural viewing c

245 Phenylephrine prevented reductions in cerebral blood flo

246 l tissue PO2 more than equi-pressor doses of phenylephrine, probably because it reduced renal oxygen

247 Phenylephrine rapidly induced CPI-17 phosphorylation fro

248 Phenylephrine regimens need to be developed that can rel

249 Pretreatment with a vasoconstrictor, phenylephrine, resulted in a reversal of the effect of Y

250 sting myocardial blood flow and EPI, HED and phenylephrine retention were homogeneous in healthy volu

251 ct cardiovascular health, better evidence on phenylephrine's effects on HR and BP is required.

252 levation of cerebral perfusion pressure with phenylephrine sex dependently prevents impairment of cer

253 ncreased cerebral perfusion pressure through phenylephrine sex dependently reduces impairment of cere

254 glucagon or Ca(2+)-mobilizing agents such as phenylephrine show an increase in their adenine nucleoti

255 Mouse hearts exposed to phenylephrine show selective CaMKIIdelta activation in t

256 stance arteries were analyzed in response to phenylephrine, sodium nitroprusside, or acetylcholine wi

257 Furthermore, ET-1(1-31) but not phenylephrine stimulated production of the TXA2 metaboli

258 Phenylephrine stimulated small cholangiocyte proliferati

259 Phenylephrine stimulated the Ca(2+) -dependent DNA-bindi

260 Phenylephrine stimulated the production of intracellular

261 GATA4 and cardiac hypertrophic responses in phenylephrine-stimulated cardiomyocytes, whereas knockdo

262 ved from Fluo-4 fluorescence measurements in phenylephrine-stimulated Flp293 cells.

263 Phenylephrine-stimulated free intracellular calcium was

264 The P2X(7) antagonist A438079 blocked the phenylephrine-stimulated increase in [Ca(2+)](i) but not

265 the level of phosphorylation is increased by phenylephrine stimulation accompanied by increased level

266 Furthermore, in response to phenylephrine stimulation, PRMT5 translocates into the c

267 y the alpha-adrenergic receptor (AR) agonist phenylephrine, suggesting inhibition of alpha-AR signali

268 Washout was only observed for phenylephrine (T(1/2) 49+/-6 min).

269 of 5 mm Hg or higher in at least 1 eye; (2) phenylephrine testing identified eyes at high risk for d

270 Parma, Italy, 72 patients with PDS underwent phenylephrine testing.

271 a hypo-contractile phenotype in response to phenylephrine that was abolished when vessels were incub

272 t cardiomyocytes induced to hypertrophy with phenylephrine, the adenosine analogue 2-chloroadenosine

273 In vitro studies using phenylephrine-treated neonatal rat ventricular myocytes,

274 A prolonged phenylephrine treatment also resulted in an increase of

275 e in cell size of cardiac myocytes following phenylephrine treatment.

276 phorylation and Akt activation in vivo after phenylephrine treatment.

277 including transverse aortic constriction and phenylephrine treatment.

278 g search terms: topical, ocular, ophthalmic, phenylephrine, tropicamide, cardiovascular effect, side

279 time of measurement or the concentration of phenylephrine used were excluded.

280 However, with phenylephrine vs. arginine vasopressin, intracranial pre

281 surized thoracodorsal resistance arteries to phenylephrine was decreased significantly by multiple Pa

282 The decrease in EIVPD induced by phenylephrine was inversely related to baseline systolic

283 Constriction to phenylephrine was not affected by 25 mM, but was decreas

284 ient, and pupillary supersensitivity to 2.5% phenylephrine was not observed.

285 52.0%-58.4%) in the second quarter of 2011; phenylephrine was the most frequently used alternative v

286 ith trimethaphan (3-7 mg min(1)), continuous phenylephrine was titrated to restore blood pressure to

287 ensitized force and activation of RhoA, when phenylephrine was used as an agonist.

288 Phenylephrine was well tolerated and there were no obser

289 Phenylephrine washout was not different from healthy vol

290 high glucose on reactivity to carbachol and phenylephrine were determined.

291 on or volume expansion; pressor responses to phenylephrine were enhanced and baroreflexes impaired in

292 Contractions evoked by ET-1(1-31), but not phenylephrine, were reduced by inhibition of cyclooxygen

293 paired contraction of vessels in response to phenylephrine, whereas MPs from healthy controls or from

294 OS)-generating hypertrophic stimuli, such as phenylephrine, whereas they are reduced by Trx1.

295 ereas defect of a third catecholamine, (11)C-phenylephrine, which is sensitive to metabolic degradati

296 o dilate rat aorta strips precontracted with phenylephrine with a NO-dependent mechanism.

297 r response to Ang II; however, coinfusion of phenylephrine with Ang II, which restored the Ang II pre

298 ll (but not large) cholangiocytes respond to phenylephrine with increased proliferation via the activ

299 hosphate (BzATP) or the alpha(1D)-AR agonist phenylephrine with or without antagonist preincubation.

300 duced by the alpha(1)-adrenoreceptor agonist phenylephrine, without affecting activation of the ERK/R