ライフサイエンスコーパス: nitroprusside

1 nding, and large intravenous doses of sodium nitroprusside.

2 ndently to bradykinin, adenosine, and sodium nitroprusside.

3 ed dilation without altering the response to nitroprusside.

4 t to endothelium-independent NO donor sodium nitroprusside.

5 f the endothelium-independent agonist sodium nitroprusside.

6 elaxation induced by either NS1619 or sodium nitroprusside.

7 of hemodynamic measurements before and after nitroprusside.

8 d to maximal vasodilatation via 28 mM sodium nitroprusside.

9 d to maximal vasodilatation via 28 mm sodium nitroprusside.

10 porine, the Ca(2+).P(i) ion pair, and sodium nitroprusside.

11 and 0.9-microg/kg boluses) of intracoronary nitroprusside.

12 nsfected with CCTeta and treated with sodium nitroprusside.

13 NG-nitro-l-arginine methyl ester and sodium nitroprusside.

14 flow to intra-arterial bradykinin and sodium nitroprusside.

15 relaxation in response to acetylcholine and nitroprusside.

16 in resting muscles with papaverine or sodium nitroprusside.

17 inhibitor, L-NAME, and the NO donor, sodium nitroprusside.

18 abrachial infusions of bradykinin and sodium nitroprusside.

19 (G)-nitro-L-arginine methyl ester and sodium nitroprusside.

20 d differences in the FBF responses to sodium nitroprusside.

21 ficantly influence responses to verapamil or nitroprusside.

22 micked by the nitric oxide (NO) donor sodium nitroprusside.

23 n endothelium-independent dilation to sodium nitroprusside.

24 ht on how H2S is understood to interact with nitroprusside.

25 clearly show a therapeutic effect of sodium nitroprusside.

26 +/-5 to 29+/-6 mm Hg; P=0.02) increased with nitroprusside.

27 below normal levels by an infusion of sodium nitroprusside.

28 o a subthreshold dose of the NO-donor sodium nitroprusside (0.1 mg/kg) following dural CGRP.

29 formed with both intracoronary adenosine and nitroprusside (0.6 microg/kg).

30 of apelin-36, (Pyr(1))apelin-13, and sodium nitroprusside (0.6 nmol/min).

31 Intracoronary nitroprusside (0.9 microg/kg) decreased systolic blood p

32 The responses to sodium nitroprusside (1 microg (100 ml tissue)(-1) min(-1)) wer

33 +/- 0.8 vs. 5.4 +/- 0.8 nl s(1)) with sodium nitroprusside (10 microM) were attenuated >60% (P < 0.05

34 endothelium-independent vasodilator, sodium nitroprusside (10(-4) M), were unchanged pre- and post-C

35 donor controls, whereas responses to sodium nitroprusside (10(-4)-10(-9) M) were similar among the g

36 Treatment with PE (10(-5) m) or sodium nitroprusside (10(-5) m) induced a significant increase

37 ereas treatment with PE (10(-5) m) or sodium nitroprusside (10(-5) m) induced a significant increase

38 nin (10(-10.5) to 10(-6.5) mol/L) and sodium nitroprusside (10(-9) to 10(-5) mol/L) was assessed by i

39 rdipine (15%), hydralazine (15%), and sodium nitroprusside (13%).

40 esuscitation-treated animals received sodium nitroprusside (2 mg) after 1 min of cardiopulmonary resu

41 , acetylcholine (5 to 20 microg/min), sodium nitroprusside (2 to 8 microg/min), and verapamil (10 to

42 etylcholine (5 to 20 microg/min), and sodium nitroprusside (2 to 8 microg/min).

43 adykinin (100 to 1,000 pmol/min), and sodium nitroprusside (2 to 8 mug/min).

44 Here we report that NO donors (sodium nitroprusside, 2',2'-(hydroxynitrosohydrazono)bis-ethani

45 st endothelium-dependent function and sodium nitroprusside (20 micro g/min) and adenosine (2.2 mg/min

46 conductance (CVC) at each site (28 mm sodium nitroprusside; 43 degrees C).

47 ized, blinded), with concomitant infusion of nitroprusside (50 microg/min, 6.4 minutes) to increase g

48 was altered by infusions of phenylephrine or nitroprusside (+/-60 mmHg over 60-90 s) in rats treated

49 us -34+/-4%; P=0.01), as was the response to nitroprusside (86+/-21% versus 171+/-22%; P=0.008).

50 ], coinfused with nitric oxide donor, sodium nitroprusside [90 to 900 ng/min]), or a single oral dose

51 Further, humans treated with nitroprusside, a drug that releases nitric oxide and cya

52 c activity of Tanshinone IIA, because sodium nitroprusside, a GSK3beta activator, largely offset its

53 BDL-CSA transport was also reduced by sodium nitroprusside, a NO donor, and by phorbol ester, a prote

54 After the infusion of sodium nitroprusside, a rapid (within 4 hours) improvement of s

55 pulmonary resuscitation that includes sodium nitroprusside, active compression-decompression cardiopu

56 matosensory stimulation, the NO donor sodium nitroprusside, added within the range of physiological c

57 measurements compared with adenosine, sodium nitroprusside also appears to be a suitable hyperemic st

58 During hypoxia, nebulized nitroprusside also reduced pulmonary artery pressure fro

59 low concentrations of 8-bromo-cGMP or sodium nitroprusside (an NO donor).

60 hange in the vasodilatory response to sodium nitroprusside, an endothelium-independent nitric oxide d

61 sumption and vasodilator responses to sodium nitroprusside, an endothelium-independent vasodilator.

62 Sodium nitroprusside, an NO donor as well, also increases iNOS

63 In m Lepr(db) control mice, sodium nitroprusside and acetylcholine induced dose-dependent v

64 The NO donors sodium nitroprusside and dipropylenetriamine NONOate were able

65 inhibited by the NO-liberating agent sodium nitroprusside and dipropylenetriamine NONOate, whereas t

66 Responses to nitroprusside and L-NMMA were not significantly differen

67 es were assessed using sequential boluses of nitroprusside and phenylephrine (modified Oxford techniq

68 Sequential nitroprusside and phenylephrine (modified Oxford test) w

69 two trials of sequential bolus injections of nitroprusside and phenylephrine in 14 young healthy subj

70 during sequential bolus injections of sodium nitroprusside and phenylephrine in 22 young, 21 older se

71 was assessed after administration of sodium nitroprusside and phenylephrine.

72 performed for an AHB-based buffer, and both nitroprusside and Raman tests confirmed the formation of

73 e mimicked by the nitric oxide donors sodium nitroprusside and spermine NONOate, suggesting a role fo

74 aggregation by the nitric oxide donor sodium nitroprusside and the phosphodiesterase 5 inhibitor sild

75 response both to acetylcholine and to sodium nitroprusside and the responses were similar in vessels

76 otected against cell death induced by sodium nitroprusside and TNFalpha plus actinomycin D and preven

77 Nitroprusside and verapamil are more potent than adenosi

78 intravenous vasodilators (ie, nitroglycerin, nitroprusside), and intravenous inotropes (ie, dobutamin

79 er exposure to the nitric oxide donor sodium nitroprusside, and betaine was able to rescue H3K4me3 le

80 vascular reactivity to acetylcholine, sodium nitroprusside, and heat.

81 a-arterial infusion of acetylcholine, sodium nitroprusside, and N(G)-monomethyl-L-arginine (L-NMMA).

82 r intra-arterial infusions of acetylcholine, nitroprusside, and the NO synthase inhibitor NG-monometh

83 s to selective receptor blockade, adenosine, nitroprusside, and verapamil against the aspirate-induce

84 nfusion of acetylcholine, bradykinin, sodium nitroprusside, and verapamil.

85 110 bpm; (3) during intravenous infusion of nitroprusside; and (4) during intravenous dobutamine inf

86 ce plus abdominal binding and 2 mg of sodium nitroprusside at 1, 4, and 8 minutes of cardiopulmonary

87 After six hours of therapy with nitroprusside (at which time the dose had been increased

88 Importantly, sodium nitroprusside attenuated C. jejuni-induced colitis in Il

89 duced to a similar extent in each group with nitroprusside, but the drop in systemic arterial pressur

90 idence interval, 5 to 48; P=0.01), to sodium nitroprusside by 20% (95% confidence interval, 3 to 40;

91 usible reaction scheme has been proposed for nitroprusside catalysis in indophenol reaction.

92 synaptosomes with H2O2, diamide, and sodium nitroprusside caused aggregation of CaMKII through forma

93 (Pyr(1))apelin-13, acetylcholine, and sodium nitroprusside caused forearm vasodilatation in patients

94 Although bradykinin and sodium nitroprusside caused similar vasodilation, SFLLRN-induce

95 Although sodium nitroprusside caused venodilation (p < 0.0001), apelin-3

96 The effects of rotenone and sodium nitroprusside (complex inhibitors of the respiratory cha

97 (P<0.01), and 5- hydroxytrytamine and sodium nitroprusside did not evoke an increase in coronary flow

98 lation by measuring acetylcholine and sodium nitroprusside dose responses.

99 othelial t-PA release, bradykinin and sodium nitroprusside dose-response curves were repeated in the

100 alf-maximal vasodilation were comparable for nitroprusside (+E, 3.3x10(-8); -E, 1.9x10(-8) mol/L) and

101 Endothelium-independent dilatation to sodium nitroprusside (EID), was not altered by age or sirtinol

102 , while iontophoresis of the NO donor sodium nitroprusside eliminated the observed differences.

103 oses) of acetylcholine (ACh; EDD) and sodium nitroprusside (endothelial-independent dilation) before

104 from fasting blood, skin responses to sodium nitroprusside (endothelium independent) and acetylcholin

105 diopulmonary resuscitation (n = 8) or sodium nitroprusside-enhanced cardiopulmonary resuscitation (n

106 mpedance threshold device (n = 6), or sodium nitroprusside-enhanced cardiopulmonary resuscitation (n

107 domized to three different protocols: sodium nitroprusside-enhanced cardiopulmonary resuscitation (n=

108 Sodium nitroprusside-enhanced cardiopulmonary resuscitation con

109 d untreated ventricular fibrillation, sodium nitroprusside-enhanced cardiopulmonary resuscitation dem

110 The addition of epinephrine to sodium nitroprusside-enhanced cardiopulmonary resuscitation dur

111 This study demonstrates that sodium nitroprusside-enhanced cardiopulmonary resuscitation fac

112 cardiopulmonary resuscitation in the sodium nitroprusside-enhanced cardiopulmonary resuscitation gro

113 cardiopulmonary resuscitation in the sodium nitroprusside-enhanced cardiopulmonary resuscitation gro

114 s with pulseless electrical activity, sodium nitroprusside-enhanced cardiopulmonary resuscitation inc

115 Sodium nitroprusside-enhanced cardiopulmonary resuscitation inc

116 his study was to assess the effect of sodium nitroprusside-enhanced cardiopulmonary resuscitation on

117 and 35+/-5 mL/min in the control and sodium nitroprusside-enhanced cardiopulmonary resuscitation plu

118 cardiopulmonary resuscitation (n=8), sodium nitroprusside-enhanced cardiopulmonary resuscitation plu

119 Control and sodium nitroprusside-enhanced cardiopulmonary resuscitation plu

120 onary resuscitation versus control or sodium nitroprusside-enhanced cardiopulmonary resuscitation plu

121 In pigs, sodium nitroprusside-enhanced cardiopulmonary resuscitation sig

122 re of 35 degrees C was decreased with sodium nitroprusside-enhanced cardiopulmonary resuscitation ver

123 We hypothesize that sodium nitroprusside-enhanced cardiopulmonary resuscitation wil

124 We hypothesized that sodium nitroprusside-enhanced cardiopulmonary resuscitation wou

125 at the addition of epinephrine during sodium nitroprusside-enhanced cardiopulmonary resuscitation wou

126 shold device, and abdominal pressure (sodium nitroprusside-enhanced cardiopulmonary resuscitation) ha

127 hanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

128 ation+adenosine, or controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

129 ectively (p<.01 for controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

130 hanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

131 tion+adenosine, and controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

132 hanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

133 ation+adenosine, or controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

134 After 1 min of sodium nitroprusside-enhanced cardiopulmonary resuscitation, ad

135 andard cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation, so

136 Sodium nitroprusside-enhanced cardiopulmonary resuscitation, so

137 andard cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation, so

138 ther reduce reperfusion injury during sodium nitroprusside-enhanced cardiopulmonary resuscitation, we

139 Sodium nitroprusside-enhanced cardiopulmonary resuscitation-tre

140 and end-tidal CO2 were increased with sodium nitroprusside-enhanced cardiopulmonary resuscitation.

141 spread throughout the first 3 mins of sodium nitroprusside-enhanced cardiopulmonary resuscitation.

142 In contrast, focal delivery of sodium nitroprusside evoked similar local dilations without Ca(

143 intervention in ICM patients, whereas sodium nitroprusside-evoked responses were similar.

144 ystemic hemodynamic effects of intracoronary nitroprusside have yet to be determined in humans.

145 did not alter relaxation responses to sodium nitroprusside, iloprost, or the K(+) channel activators

146 to phenylephrine, acetylcholine, and sodium nitroprusside improved after Aza in HHcy mice.

147 We determined the response to intravenous nitroprusside in 25 patients with severe aortic stenosis

148 abrachial infusions of bradykinin and sodium nitroprusside in 33 sedentary adults: 10 normal-weight (

149 h is becoming a viable alternative to sodium nitroprusside in children.

150 ontrary, in 16 hypertensive patients, sodium nitroprusside in equidepressor doses induced a significa

151 ine the acute hemodynamic response to sodium nitroprusside in LGSAS with preserved EF.

152 junction potentials and responses to sodium nitroprusside in murine colonic muscles.

153 nses to vasodilation with intravenous sodium nitroprusside in patients with HFrEF (n = 174) and HFpEF

154 sing bolus doses of phenylephrine and sodium nitroprusside, in anaesthetized male Wistar rats at a co

155 Intracoronary nitroprusside, in doses commonly used for the treatment

156 itroso-N-acetyl-dl-penacillamine, and sodium nitroprusside, inactivated both isoforms in a dose-depen

157 Nitroprusside increased sympathetic outflow significantl

158 In contrast, sodium nitroprusside induced similar relaxations in the two exp

159 hat aortas have significantly blunted sodium nitroprusside-induced (NO-dependent) vasorelaxation and

160 Acetylcholine-induced and sodium nitroprusside-induced dilation in resistance arteries wa

161 blunted compared with lean rats, but sodium nitroprusside-induced dilation was comparable.

162 athetic nerve activity response to transient nitroprusside-induced hypotension (53.3 +/- 3.7 vs. 40.1

163 before, during and after a 10 min period of nitroprusside-induced hypotension.

164 and 9 control subjects at rest and during a nitroprusside-induced hypotensive stimulus.

165 After 24 hours of nitroprusside infusion (dose, 128+/-96 microg per minute

166 hange during baseline measurements or during nitroprusside infusion but decreased during pacing (from

167 Under nitroprusside infusion, a neurovascular-coupling inhibit

168 mal vasodilatation achieved via 28 mm sodium nitroprusside infusion.

169 ing (T(loc) = 43 degrees C) and 28 mM sodium nitroprusside infusion.

170 r after bradykinin, acetylcholine and sodium nitroprusside infusions (p < 0.001), but this was unaffe

171 Cs into neurons, whereas the NO donor sodium nitroprusside inhibited NPC proliferation and increased

172 tion, but the nitric oxide (NO) donor sodium nitroprusside initiated biphasic rises.

173 Sodium nitroprusside is one of several agents considered effect

174 Treatment with sodium nitroprusside led to increases in the phosphorylation of

175 lized to maximal CVC (CVCmax, 28.0 mM sodium nitroprusside + local heating to 43 degrees C).

176 zed to maximal CVC (%CVC(max)) (28 mm sodium nitroprusside + local heating to 43 degrees C).

177 ssessed in response to acetylcholine, sodium nitroprusside, local heating (42 degrees C), and to nonn

178 However, vasodilators such as nitroprusside may improve myocardial performance if peri

179 d metal-nitrosyl linkage isomerism in sodium nitroprusside (Na(2)[Fe(II)(CN)(5)NO].2H(2)O, SNP) disso

180 ca have recommended consideration for use of nitroprusside, nitroglycerin, or nesiritide in addition

181 Neither injection of the vasodilator sodium nitroprusside nor blood withdrawal from the superior ven

182 oline) and -independent vasodilation (sodium nitroprusside) of isolated, pressurized coronary small a

183 O when adding gas or the (*)NO donor, sodium nitroprusside, on injection into plant leaves, was demon

184 ation of 10(-4) M adenosine, 10(-4) M sodium nitroprusside or 10(-5) M pinacidil directly to capillar

185 CH (P=0.009) but not the responses to sodium nitroprusside or adenosine.

186 +/-5%, P<0.01) but was not altered to sodium nitroprusside or bradykinin.

187 human corneal cells was induced with sodium nitroprusside or camptothecin and activation of prothrom

188 lase-cyclic GMP-protein-kinase-G system with nitroprusside or membrane-permeant cyclic GMP analogs mi

189 Injection of sodium nitroprusside or selective PKG activators into the later

190 n response to stimulation with either sodium nitroprusside or sphingosine 1-phosphate.

191 y treatment with the nitric oxide (NO) donor nitroprusside or the ATP-sensitive potassium (K(ATP)) ch

192 nalyzed in response to phenylephrine, sodium nitroprusside, or acetylcholine with or without inhibito

193 experience a reduction in stroke volume with nitroprusside (p < 0.0001), suggesting greater vulnerabi

194 All measures of afterload were reduced with nitroprusside (P<0.001 for all).

195 (P<0.05), acetylcholine (P<0.05), and sodium nitroprusside (P<0.001) infusions 2 hours after exposure

196 esponse to acetylcholine (P=0.01) and sodium nitroprusside (P=0.004).

197 01) without affecting the response to sodium nitroprusside (P=0.31).

198 ne (P=0.01) but not apelin (P=0.3) or sodium nitroprusside (P=0.9) was attenuated in patients with he

199 ne, combined fetal treatment with L-NAME and nitroprusside prevents generalized vasoconstriction and

200 blunted compared with m Lepr(db), but sodium nitroprusside produced comparable dilation.

201 Intracoronary nitroprusside produced equivalent coronary hyperemia wit

202 bradykinin (BK) were similar, whereas sodium nitroprusside produced maximal dilation locally without

203 Both inhaled nitric oxide and nebulized nitroprusside produced prompt, significant, selective re

204 Compared with adenosine, intracoronary nitroprusside produces an equivalent but more prolonged

205 ule-1 and blood flow responses to L-NMMA and nitroprusside (r=0.53, P=0.004 and r=-0.66, P<0.001, res

206 Nitroprusside rapidly and markedly improves cardiac func

207 In all patients, nitroprusside reduced elastance, left ventricular fillin

208 Treatment with the NO donor sodium nitroprusside reduced levels of HIF-1alpha, whereas NO d

209 Nitroprusside reduced mean pulmonary artery pressure (25

210 Nitroprusside reduces afterload and left ventricular fil

211 extracts showed capacity to scavenge sodium nitroprusside-released nitric oxide (NO), RM being more

212 ent vasodilation to acetylcholine and sodium nitroprusside, respectively.

213 Sodium nitroprusside response was unchanged by all treatments.

214 onors dipropylenetriamine NONOate and sodium nitroprusside showed opposite effects.

215 upon exposure to H(2)O(2), but not to sodium nitroprusside, SIN-1, and DETA-NO.

216 (20 mM; to inhibit NOS activity) and sodium nitroprusside (SNP 10 microM) were infused by microdialy

217 ction relative to adenosine (ADO) and sodium nitroprusside (SNP) (PE-mediated DeltaFVC: ATP: -16 +/-

218 cy of postharvest dip treatment donor sodium nitroprusside (SNP) 0.000, 0.001, 0.002 and 0.003 mol L(

219 ects observed upon the application of sodium nitroprusside (SNP) and H2S can be ascribed to the gener

220 ood pressure (BP) induced by stepwise sodium nitroprusside (SNP) and phenylephrine (PhE) infusion.

221 P) induced by intravenous infusion of sodium nitroprusside (SNP) and phenylephrine.

222 sulin alone (Control) or insulin plus sodium nitroprusside (SNP) at variable rate to double leg blood

223 a-arterial infusions of ACh, ATP, and sodium nitroprusside (SNP) before and during ascorbic acid (AA)

224 ponsiveness to phenylephrine (PE) and sodium nitroprusside (SNP) decreased over time for artery rings

225 h study day, 3 acetylcholine (ACh) or sodium nitroprusside (SNP) dose-response studies were performed

226 tment blocked, whereas L-arginine and sodium nitroprusside (SNP) each enhanced, EC uptake of fluoresc

227 to examine the safety and efficacy of sodium nitroprusside (SNP) for patients with acute decompensate

228 ical stressor [hemodynamic stress via sodium nitroprusside (SNP) i.v.] on stimulus evoked responses o

229 The NO donor sodium nitroprusside (SNP) increased intracellular Ca(2+) wave

230 ted whether activation of GSK3beta by sodium nitroprusside (SNP) mitigates kidney injury in diabetes.

231 the effects of nitric oxide (NO) and sodium nitroprusside (SNP) on Bacillus subtilis physiology and

232 with control subjects (P=0.002), but sodium nitroprusside (SNP) responses were not (P=0.3).

233 Exposure to the NO donor sodium nitroprusside (SNP) showed that high NO levels suppresse

234 e endothelium-independent vasodilator sodium nitroprusside (SNP) were examined.

235 ) inhibited purified sGC activated by sodium nitroprusside (SNP), a precursor of nitric oxide (NO), e

236 ) recovery was partially inhibited by sodium nitroprusside (SNP), an NO donor, and l-arginine, the en

237 ro-N-acetyl-d,l-penicillamine (SNAP), sodium nitroprusside (SNP), and hydrogen peroxide than were MS

238 dministration of another vasodilator, sodium nitroprusside (SNP), may equally improve CBF and cerebra

239 given a 1-mL bolus injection of GTN, sodium nitroprusside (SNP), or adenosine through a catheter in

240 Here we show that the NO donor, sodium nitroprusside (SNP), rapidly represses c-myc gene transc

241 ulation, but infusion of the NO donor sodium nitroprusside (SNP), so as to similarly reduce baseline

242 tophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP), were negatively correlated with per

243 olus doses of the nitric oxide donor, sodium nitroprusside (SNP), were studied.

244 usion of exogenous NO, in the form of sodium nitroprusside (SNP), would fully restore vasodilatation

245 695, Thr696 and Thr853 in response to sodium nitroprusside (SNP)-induced relaxation in denuded rabbit

246 in human brain endothelial cells with sodium nitroprusside (SNP).

247 ere sensitized by GSK3beta activator, sodium nitroprusside (SNP).

248 ion caused by the nitric oxide donor, sodium nitroprusside (SNP).

249 pplication of acetylcholine (ACh) and sodium nitroprusside (SNP).

250 , 3-morpholinosydnonimine (SIN-1), or sodium nitroprusside (SNP).

251 Microinjection of the NO donor sodium nitroprusside (SNP, 1 mM, 50 nl) at a cardioinhibitory s

252 The NO donor sodium nitroprusside (SNP, 10 mM) stimulates additional cGMP pr

253 trus roots with NaHS (a H2S donor) or sodium nitroprusside (SNP, a NO donor) for 2 days (d) could eli

254 oline (ACh; 1 x 10(9)-1 x 10(5)m) and sodium nitroprusside (SNP; 1 x 10(9)-1 x 10(4)m), constrictor r

255 ylpenicillamine (SNAP; 50 microM) and sodium nitroprusside (SNP; 100 microM) did not change the gener

256 In eight subjects increasing doses of sodium nitroprusside (SNP; 8.4 x 10(-6)-8.4 x 10(-3)m) were adm

257 (ACh; endothelium dependent) but not sodium nitroprusside (SNP; endothelium independent).

258 (5% maximum voluntary contraction) or sodium nitroprusside (SNP; endothelium-independent dilator) whi

259 endothelium-independent vasodilator (sodium nitroprusside, SNP), or potassium chloride (KCl) at rest

260 ME); low-dose NO infusion (1.0 microM sodium nitroprusside, SNP); adrenergic blockade (10 mM bretyliu

261 city of vascular smooth muscle cells (sodium nitroprusside; SNP).

262 ore, CCTeta had no effect on basal or sodium nitroprusside-stimulated alphabeta(Cys-105) sGC, a const

263 Sodium nitroprusside stimulation of the cGMP-generating cyclase

264 taneous vasodilatation in response to sodium nitroprusside, suggesting that ET-1 diminishes the dilat

265 fore therapy (A), after initial diuretic and nitroprusside therapy to optimize hemodynamics (B, mean

266 The effect of nitroprusside to antagonize UK 14,304 responses was prev

267 by i.v. injection of phenylephrine or sodium nitroprusside to increase or decrease arterial blood pre

268 c and hemodynamic responses of intracoronary nitroprusside to intracoronary adenosine in patients dur

269 eart received infusion of intravenous sodium nitroprusside to reduce blood pressure and arterial afte

270 t that 1) the ability of the NO donor sodium nitroprusside to reduce blood pressure is impaired in RG

271 ide toxicity and prophylactic measure during nitroprusside treatment, inosine may serve as a biomarke

272 Change in SVI with nitroprusside varied inversely to baseline SVI and demon

273 ne and substance P) and -independent (sodium nitroprusside) vasodilators were measured in eight healt

274 blood pressure (baroreflex activation) with nitroprusside, venous NE concentration increased to the

275 ters was increased to 43 degrees C and 28 mm nitroprusside was infused to achieve maximal vasodilatat

276 The nitric oxide (NO) donor sodium nitroprusside was injected intraperitoneally (2 mg/kg da

277 rt rate to transient hypotension with sodium nitroprusside was normalized by 66% compared with CHF co

278 ls to endothelium-independent agonist sodium nitroprusside was not altered, the endothelium-dependent

279 At the end of each protocol, 56 mm sodium nitroprusside was perfused at microdialysis sites to rai

280 re locally heated to 43 degrees C and sodium nitroprusside was perfused to elicit maximal vasodilatat

281 Maximal relaxation to sodium nitroprusside was similar in aorta from normal and LPS-t

282 ry action of both carbamylcholine and sodium nitroprusside was ultimately dependent on muscarinic rec

283 n to endothelium-independent NO donor sodium nitroprusside was unaffected after all time periods of i

284 e endothelium-independent vasodilator sodium nitroprusside was unaffected by AGE-Glu.

285 dothelium-independent vasodilation to sodium nitroprusside was unaffected.

286 hereas direct vessel relaxation using sodium nitroprusside was unaltered.

287 bitor NG-monomethyl-L-arginine (L-NMMA); and nitroprusside was used to assess sensitivity to nitric o

288 Nitroprusside was well tolerated and had minimal side ef

289 (responses to acetylcholine [ACH] and sodium nitroprusside) was tested in the SUMMIT study.

290 ine or the fall in pressure evoked by sodium nitroprusside, was significantly attenuated in depleted

291 sion of acetylcholine, substance P or sodium nitroprusside were 25 +/- 4, 30 +/- 7 and 29 +/- 5 ml mi

292 elaxation responses to bradykinin and sodium nitroprusside were assessed at days 5 and 10 postinfecti

293 es to intrabrachial acetylcholine and sodium nitroprusside were assessed using venous occlusion pleth

294 FFR measurements with intracoronary nitroprusside were identical to those obtained with intr

295 Acetylcholine and sodium nitroprusside were iontophoresed into the forearm skin.

296 (P < 0.05) to the nitric oxide donor sodium nitroprusside were reduced in protein-restricted group f

297 ose-response curves to bradykinin and sodium nitroprusside were repeated with a coinfusion of the ant

298 s, vasorelaxation responses to BK and sodium nitroprusside were similar before and 219+/-37 days afte

299 Responses to acetylcholine, but not sodium nitroprusside, were impaired in patients with diabetes (

300 very strongly induced in response to sodium nitroprusside, which indicates its involvement in stress