ライフサイエンスコーパス: sodium nitroprusside

1 se dependently to bradykinin, adenosine, and sodium nitroprusside.

2 but not to endothelium-independent NO donor sodium nitroprusside.

3 ct on relaxation induced by either NS1619 or sodium nitroprusside.

4 usion of the endothelium-independent agonist sodium nitroprusside.

5 rmalized to maximal vasodilatation via 28 mM sodium nitroprusside.

6 rmalized to maximal vasodilatation via 28 mm sodium nitroprusside.

7 staurosporine, the Ca(2+).P(i) ion pair, and sodium nitroprusside.

8 bly transfected with CCTeta and treated with sodium nitroprusside.

9 tion of NG-nitro-l-arginine methyl ester and sodium nitroprusside.

10 plasma flow to intra-arterial bradykinin and sodium nitroprusside.

11 evels) in resting muscles with papaverine or sodium nitroprusside.

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

13 to intrabrachial infusions of bradykinin and sodium nitroprusside.

14 on of N(G)-nitro-L-arginine methyl ester and sodium nitroprusside.

15 -related differences in the FBF responses to sodium nitroprusside.

16 ol/L), bradykinin, adenosine, pinacidil, and sodium nitroprusside.

17 s reduced via steady-state administration of sodium nitroprusside.

18 n be mimicked by the nitric oxide (NO) donor sodium nitroprusside.

19 ANOVA) but had no effect on the response to sodium nitroprusside.

20 y to the endothelium-independent vasodilator sodium nitroprusside.

21 (ACH), L-NG monomethyl arginine (L-NMMA) and sodium nitroprusside.

22 MitoQ on endothelium-independent dilation to sodium nitroprusside.

23 results clearly show a therapeutic effect of sodium nitroprusside.

24 sed to below normal levels by an infusion of sodium nitroprusside.

25 inal binding, and large intravenous doses of sodium nitroprusside.

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

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

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

29 n (2.0 +/- 0.8 vs. 5.4 +/- 0.8 nl s(1)) with sodium nitroprusside (10 microM) were attenuated >60% (P

30 to the endothelium-independent vasodilator, sodium nitroprusside (10(-4) M), were unchanged pre- and

31 ICM and donor controls, whereas responses to sodium nitroprusside (10(-4)-10(-9) M) were similar amon

32 Treatment with PE (10(-5) m) or sodium nitroprusside (10(-5) m) induced a significant in

33 MCs, whereas treatment with PE (10(-5) m) or sodium nitroprusside (10(-5) m) induced a significant in

34 Sodium nitroprusside (10(-6) or 10(-5) m) and 8-Br-cGMP

35 bradykinin (10(-10.5) to 10(-6.5) mol/L) and sodium nitroprusside (10(-9) to 10(-5) mol/L) was assess

36 by nicardipine (15%), hydralazine (15%), and sodium nitroprusside (13%).

37 onary resuscitation-treated animals received sodium nitroprusside (2 mg) after 1 min of cardiopulmona

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

39 in), acetylcholine (5 to 20 microg/min), and sodium nitroprusside (2 to 8 microg/min).

40 in), bradykinin (100 to 1,000 pmol/min), and sodium nitroprusside (2 to 8 mug/min).

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

42 red after L-NAME by infusion of the NO donor sodium nitroprusside (20 g x kg(-1) x min(-1).

43 ) to test endothelium-dependent function and sodium nitroprusside (20 micro g/min) and adenosine (2.2

44 tracoronary acetylcholine 15 microg/min) and sodium nitroprusside (20 microg/min) were administered t

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

46 to 40 pmol/min; endothelium-dependent), and sodium nitroprusside (5 to 20 microgram/min; endothelium

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

48 rapeutic activity of Tanshinone IIA, because sodium nitroprusside, a GSK3beta activator, largely offs

49 NBDL-CSA transport was also reduced by sodium nitroprusside, a NO donor, and by phorbol ester,

50 After the infusion of sodium nitroprusside, a rapid (within 4 hours) improveme

51 in the presence of both LHRH and AA, whereas sodium nitroprusside, a releaser of NO, stimulated LH an

52 stimulation of l-arginine transport whereas sodium nitroprusside activated an outward potassium curr

53 cardiopulmonary resuscitation that includes sodium nitroprusside, active compression-decompression c

54 s to somatosensory stimulation, the NO donor sodium nitroprusside, added within the range of physiolo

55 rate during post-exercise ischaemia without sodium nitroprusside administration followed a similar p

56 of FFR measurements compared with adenosine, sodium nitroprusside also appears to be a suitable hyper

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

58 as no change in the vasodilatory response to sodium nitroprusside, an endothelium-independent nitric

59 ble consumption and vasodilator responses to sodium nitroprusside, an endothelium-independent vasodil

60 Sodium nitroprusside, an NO donor as well, also increase

61 erine 351 blocked the stimulatory effects of sodium nitroprusside and 8-Br-cGMP on open probability w

62 In m Lepr(db) control mice, sodium nitroprusside and acetylcholine induced dose-depe

63 and of endothelium-independent function with sodium nitroprusside and adenosine.

64 The NO donors sodium nitroprusside and dipropylenetriamine NONOate wer

65 ere all inhibited by the NO-liberating agent sodium nitroprusside and dipropylenetriamine NONOate, wh

66 During therapy (7.3 +/- 6 days) with sodium nitroprusside and diuresis, hemodynamics improved

67 ed genes in Bacillus subtilis was induced by sodium nitroprusside and nitric oxide.

68 st and during sequential bolus injections of sodium nitroprusside and phenylephrine in 22 young, 21 o

69 pproximately 13 mmHg) by bolus injections of sodium nitroprusside and phenylephrine, respectively.

70 unction was assessed after administration of sodium nitroprusside and phenylephrine.

71 sculentum) plants was inhibited by NO donors sodium nitroprusside and S-nitroso-N-acetyl-penicillamin

72 ide were mimicked by the nitric oxide donors sodium nitroprusside and spermine NONOate, suggesting a

73 atelet aggregation by the nitric oxide donor sodium nitroprusside and the phosphodiesterase 5 inhibit

74 ted in response both to acetylcholine and to sodium nitroprusside and the responses were similar in v

75 also protected against cell death induced by sodium nitroprusside and TNFalpha plus actinomycin D and

76 sGC inhibitor LY83583 blocked the effects of sodium nitroprusside and YC-1.

77 nt (acetylcholine), endothelium-independent (sodium nitroprusside) and nitrate-independent (verapamil

78 lls after exposure to the nitric oxide donor sodium nitroprusside, and betaine was able to rescue H3K

79 ld and vascular reactivity to acetylcholine, sodium nitroprusside, and heat.

80 al intra-arterial infusion of acetylcholine, sodium nitroprusside, and N(G)-monomethyl-L-arginine (L-

81 erial infusion of acetylcholine, bradykinin, sodium nitroprusside, and verapamil.

82 Sodium nitroprusside, another NO donor also inhibited AI

83 ase in KCC1 mRNA levels after treatment with sodium nitroprusside as demonstrated by semiquantitative

84 ld device plus abdominal binding and 2 mg of sodium nitroprusside at 1, 4, and 8 minutes of cardiopul

85 Importantly, sodium nitroprusside attenuated C. jejuni-induced coliti

86 ne and endothelium-independent function with sodium nitroprusside, before and after ACE inhibition wi

87 The effects of sodium nitroprusside, but not ACH or L-NMMA, were reprod

88 5% confidence interval, 5 to 48; P=0.01), to sodium nitroprusside by 20% (95% confidence interval, 3

89 e brain synaptosomes with H2O2, diamide, and sodium nitroprusside caused aggregation of CaMKII throug

90 ons of (Pyr(1))apelin-13, acetylcholine, and sodium nitroprusside caused forearm vasodilatation in pa

91 Although bradykinin and sodium nitroprusside caused similar vasodilation, SFLLRN

92 Although sodium nitroprusside caused venodilation (p < 0.0001), a

93 The effects of rotenone and sodium nitroprusside (complex inhibitors of the respirat

94 grafts (P<0.01), and 5- hydroxytrytamine and sodium nitroprusside did not evoke an increase in corona

95 vasodilation by measuring acetylcholine and sodium nitroprusside dose responses.

96 on endothelial t-PA release, bradykinin and sodium nitroprusside dose-response curves were repeated

97 without bolus intravenous administration of sodium nitroprusside during the ischaemic period.

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

99 l ester, while iontophoresis of the NO donor sodium nitroprusside eliminated the observed differences

100 ssive doses) of acetylcholine (ACh; EDD) and sodium nitroprusside (endothelial-independent dilation)

101 oteins from fasting blood, skin responses to sodium nitroprusside (endothelium independent) and acety

102 ssure, and end-tidal CO2 were increased with sodium nitroprusside-enhanced cardiopulmonary resuscitat

103 We hypothesize that sodium nitroprusside-enhanced cardiopulmonary resuscitat

104 This study demonstrates that sodium nitroprusside-enhanced cardiopulmonary resuscitat

105 during cardiopulmonary resuscitation in the sodium nitroprusside-enhanced cardiopulmonary resuscitat

106 mL/min and 35+/-5 mL/min in the control and sodium nitroprusside-enhanced cardiopulmonary resuscitat

107 ere randomized to three different protocols: sodium nitroprusside-enhanced cardiopulmonary resuscitat

108 nhanced cardiopulmonary resuscitation (n=8), sodium nitroprusside-enhanced cardiopulmonary resuscitat

109 The addition of epinephrine to sodium nitroprusside-enhanced cardiopulmonary resuscitat

110 We hypothesized that sodium nitroprusside-enhanced cardiopulmonary resuscitat

111 Control and sodium nitroprusside-enhanced cardiopulmonary resuscitat

112 ized that the addition of epinephrine during sodium nitroprusside-enhanced cardiopulmonary resuscitat

113 during cardiopulmonary resuscitation in the sodium nitroprusside-enhanced cardiopulmonary resuscitat

114 Sodium nitroprusside-enhanced cardiopulmonary resuscitat

115 mperature of 35 degrees C was decreased with sodium nitroprusside-enhanced cardiopulmonary resuscitat

116 diopulmonary resuscitation versus control or sodium nitroprusside-enhanced cardiopulmonary resuscitat

117 im of this study was to assess the effect of sodium nitroprusside-enhanced cardiopulmonary resuscitat

118 Sodium nitroprusside-enhanced cardiopulmonary resuscitat

119 side-enhanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitat

120 suscitation+adenosine, and controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitat

121 Sodium nitroprusside-enhanced cardiopulmonary resuscitat

122 ce threshold device, and abdominal pressure (sodium nitroprusside-enhanced cardiopulmonary resuscitat

123 ther standard cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitat

124 side-enhanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitat

125 esuscitation+adenosine, or controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitat

126 To further reduce reperfusion injury during sodium nitroprusside-enhanced cardiopulmonary resuscitat

127 pauses spread throughout the first 3 mins of sodium nitroprusside-enhanced cardiopulmonary resuscitat

128 for standard cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitat

129 side-enhanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitat

130 esuscitation+adenosine, or controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitat

131 9, respectively (p<.01 for controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitat

132 After 1 min of sodium nitroprusside-enhanced cardiopulmonary resuscitat

133 rolonged untreated ventricular fibrillation, sodium nitroprusside-enhanced cardiopulmonary resuscitat

134 ard cardiopulmonary resuscitation (n = 8) or sodium nitroprusside-enhanced cardiopulmonary resuscitat

135 ion + impedance threshold device (n = 6), or sodium nitroprusside-enhanced cardiopulmonary resuscitat

136 animals with pulseless electrical activity, sodium nitroprusside-enhanced cardiopulmonary resuscitat

137 Sodium nitroprusside-enhanced cardiopulmonary resuscitat

138 In pigs, sodium nitroprusside-enhanced cardiopulmonary resuscitat

139 In contrast, focal delivery of sodium nitroprusside evoked similar local dilations with

140 F-LVAD intervention in ICM patients, whereas sodium nitroprusside-evoked responses were similar.

141 activation of cytosolic guanylyl cyclase by sodium nitroprusside had no effect on Ca2+ efflux, Ca2+

142 It did not alter relaxation responses to sodium nitroprusside, iloprost, or the K(+) channel acti

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

144 to intrabrachial infusions of bradykinin and sodium nitroprusside in 33 sedentary adults: 10 normal-w

145 e, which is becoming a viable alternative to sodium nitroprusside in children.

146 n the contrary, in 16 hypertensive patients, sodium nitroprusside in equidepressor doses induced a si

147 determine the acute hemodynamic response to sodium nitroprusside in LGSAS with preserved EF.

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

149 e responses to vasodilation with intravenous sodium nitroprusside in patients with HFrEF (n = 174) an

150 rves, using bolus doses of phenylephrine and sodium nitroprusside, in anaesthetized male Wistar rats

151 O), S-nitroso-N-acetyl-dl-penacillamine, and sodium nitroprusside, inactivated both isoforms in a dos

152 In contrast, sodium nitroprusside induced similar relaxations in the

153 howed that aortas have significantly blunted sodium nitroprusside-induced (NO-dependent) vasorelaxati

154 Acetylcholine-induced and sodium nitroprusside-induced dilation in resistance arte

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

156 - 4 beats x min(-1); P < 0.001) during bolus sodium nitroprusside-induced reductions in blood pressur

157 acute hypoxaemia protocol, withdrawal of the sodium nitroprusside infusion from fetuses undergoing th

158 to maximal vasodilatation achieved via 28 mm sodium nitroprusside infusion.

159 by heating (T(loc) = 43 degrees C) and 28 mM sodium nitroprusside infusion.

160 t manner after bradykinin, acetylcholine and sodium nitroprusside infusions (p < 0.001), but this was

161 the NPCs into neurons, whereas the NO donor sodium nitroprusside inhibited NPC proliferation and inc

162 generation, but the nitric oxide (NO) donor sodium nitroprusside initiated biphasic rises.

163 Sodium nitroprusside is one of several agents considered

164 Treatment with sodium nitroprusside led to increases in the phosphoryla

165 d normalized to maximal CVC (CVCmax, 28.0 mM sodium nitroprusside + local heating to 43 degrees C).

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

167 were assessed in response to acetylcholine, sodium nitroprusside, local heating (42 degrees C), and

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

169 (n-propyl)amino]diazen-1-ium-1, 2-dialase or sodium nitroprusside, NO donors, or a combination of xan

170 Neither injection of the vasodilator sodium nitroprusside nor blood withdrawal from the super

171 r (L-NAME, 100 mg x kg(-1)) and the NO donor sodium nitroprusside (NP, 5.1 +/- 2.0 microg x kg(-1) x

172 cetylcholine) and -independent vasodilation (sodium nitroprusside) of isolated, pressurized coronary

173 or (*)NO when adding gas or the (*)NO donor, sodium nitroprusside, on injection into plant leaves, wa

174 application of 10(-4) M adenosine, 10(-4) M sodium nitroprusside or 10(-5) M pinacidil directly to c

175 se to ACH (P=0.009) but not the responses to sodium nitroprusside or adenosine.

176 M(-) 85+/-5%, P<0.01) but was not altered to sodium nitroprusside or bradykinin.

177 ultured human corneal cells was induced with sodium nitroprusside or camptothecin and activation of p

178 f motor neurons to nitric oxide (NO) donors (sodium nitroprusside or NONOate), H2O2, or NO donor plus

179 Injection of sodium nitroprusside or selective PKG activators into th

180 inase in response to stimulation with either sodium nitroprusside or sphingosine 1-phosphate.

181 nd allopurinol treatment arms with regard to sodium nitroprusside or verapamil.

182 ulated by NO donors (diethylamine NONOate or sodium nitroprusside) or the cyclic GMP analog, 8-bromo-

183 were analyzed in response to phenylephrine, sodium nitroprusside, or acetylcholine with or without i

184 ykinin (P<0.05), acetylcholine (P<0.05), and sodium nitroprusside (P<0.001) infusions 2 hours after e

185 ood flow increased with both substance P and sodium nitroprusside (P<0.001), although coronary sinus

186 on in response to acetylcholine (P=0.01) and sodium nitroprusside (P=0.004).

187 n (P=0.01) without affecting the response to sodium nitroprusside (P=0.31).

188 ylcholine (P=0.01) but not apelin (P=0.3) or sodium nitroprusside (P=0.9) was attenuated in patients

189 Sodium nitroprusside produced a similar increase in plat

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

191 ses to bradykinin (BK) were similar, whereas sodium nitroprusside produced maximal dilation locally w

192 Treatment with the NO donor sodium nitroprusside reduced levels of HIF-1alpha, where

193 an NO/cGMP-mediating mechanism, the NO donor sodium nitroprusside reduced tau (maximal effect, -14+/-

194 he wine extracts showed capacity to scavenge sodium nitroprusside-released nitric oxide (NO), RM bein

195 ndependent vasodilation to acetylcholine and sodium nitroprusside, respectively.

196 Sodium nitroprusside response was unchanged by all treat

197 Conversely, injection of sodium nitroprusside resulted in a positive chronotropic

198 otein-caveolin-1 construct demonstrated that sodium nitroprusside resulted in the increased fluoresce

199 with cholera toxin B subunit indicated that sodium nitroprusside reversibly decreased its binding.

200 he NO donors dipropylenetriamine NONOate and sodium nitroprusside showed opposite effects.

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

202 L-NAME (20 mM; to inhibit NOS activity) and sodium nitroprusside (SNP 10 microM) were infused by mic

203 constriction relative to adenosine (ADO) and sodium nitroprusside (SNP) (PE-mediated DeltaFVC: ATP: -

204 efficacy of postharvest dip treatment donor sodium nitroprusside (SNP) 0.000, 0.001, 0.002 and 0.003

205 cal effects observed upon the application of sodium nitroprusside (SNP) and H2S can be ascribed to th

206 mean blood pressure (BP) induced by stepwise sodium nitroprusside (SNP) and phenylephrine (PhE) infus

207 ure (MAP) induced by intravenous infusion of sodium nitroprusside (SNP) and phenylephrine.

208 Apoptosis was induced by addition of sodium nitroprusside (SNP) at 1-2 mM to >80% confluent p

209 g of insulin alone (Control) or insulin plus sodium nitroprusside (SNP) at variable rate to double le

210 nt vasodilation with nitroglycerin (NTG) and sodium nitroprusside (SNP) before and after intracoronar

211 al intra-arterial infusions of ACh, ATP, and sodium nitroprusside (SNP) before and during ascorbic ac

212 nal responsiveness to phenylephrine (PE) and sodium nitroprusside (SNP) decreased over time for arter

213 On each study day, 3 acetylcholine (ACh) or sodium nitroprusside (SNP) dose-response studies were pe

214 pretreatment blocked, whereas L-arginine and sodium nitroprusside (SNP) each enhanced, EC uptake of f

215 signed to examine the safety and efficacy of sodium nitroprusside (SNP) for patients with acute decom

216 ysiological stressor [hemodynamic stress via sodium nitroprusside (SNP) i.v.] on stimulus evoked resp

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

218 Sodium nitroprusside (SNP) mimicked the actions of carba

219 We tested whether activation of GSK3beta by sodium nitroprusside (SNP) mitigates kidney injury in di

220 xamined the effects of nitric oxide (NO) and sodium nitroprusside (SNP) on Bacillus subtilis physiolo

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

222 ONOO-), 3-morpholinosydnonimine (SIN-1), and sodium nitroprusside (SNP) resulted in apoptotic cell de

223 Exposure to the NO donor sodium nitroprusside (SNP) showed that high NO levels su

224 (WRT) cells perished via apoptosis following sodium nitroprusside (SNP) treatment.

225 nnel blockers on the actions of the NO donor sodium nitroprusside (SNP) were evaluated in isolated gu

226 and the endothelium-independent vasodilator sodium nitroprusside (SNP) were examined.

227 in arteries exposed to authentic ONOO- or to sodium nitroprusside (SNP)+xanthine (XA)+xanthine oxidas

228 NO donors sodium nitroprusside (SNP), 1 mmol/L, and S-nitroso-N-ac

229 a stem cells and is suppressed by NO donors [sodium nitroprusside (SNP), 3-morpholinosydnonimine-1, a

230 ut restored when baseline FVC is restored by sodium nitroprusside (SNP), a NO donor.

231 , Ca(2+) inhibited purified sGC activated by sodium nitroprusside (SNP), a precursor of nitric oxide

232 ontraction, and the nitric oxide (NO) donor, sodium nitroprusside (SNP), all increase glucose transpo

233 e, pH(i) recovery was partially inhibited by sodium nitroprusside (SNP), an NO donor, and l-arginine,

234 oronary infusions of acetylcholine (ACH) and sodium nitroprusside (SNP), and during cold pressor test

235 o S-nitro-N-acetyl-d,l-penicillamine (SNAP), sodium nitroprusside (SNP), and hydrogen peroxide than w

236 that administration of another vasodilator, sodium nitroprusside (SNP), may equally improve CBF and

237 dog was given a 1-mL bolus injection of GTN, sodium nitroprusside (SNP), or adenosine through a cathe

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

239 of stimulation, but infusion of the NO donor sodium nitroprusside (SNP), so as to similarly reduce ba

240 little effect on that caused by the NO donor sodium nitroprusside (SNP), suggesting that acetylcholin

241 to iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP), were negatively correlated w

242 asing bolus doses of the nitric oxide donor, sodium nitroprusside (SNP), were studied.

243 ose infusion of exogenous NO, in the form of sodium nitroprusside (SNP), would fully restore vasodila

244 at Ser695, Thr696 and Thr853 in response to sodium nitroprusside (SNP)-induced relaxation in denuded

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

246 e and were sensitized by GSK3beta activator, sodium nitroprusside (SNP).

247 roxidation caused by the nitric oxide donor, sodium nitroprusside (SNP).

248 pical application of acetylcholine (ACh) and sodium nitroprusside (SNP).

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

250 Microinjection of the NO donor sodium nitroprusside (SNP, 1 mM, 50 nl) at a cardioinhib

251 The NO donor sodium nitroprusside (SNP, 10 mM) stimulates additional

252 t of citrus roots with NaHS (a H2S donor) or sodium nitroprusside (SNP, a NO donor) for 2 days (d) co

253 centrations of TRAIL (12.5-200 ng/ml) and/or sodium nitroprusside (SNP; 0.03-1 mM) for 12 h.

254 holine (ACh; 7.5, 15, and 30 microg/min) and sodium nitroprusside (SNP; 0.8,1.6, and 3.2 microg/min)

255 cetylcholine (ACh; 1 x 10(9)-1 x 10(5)m) and sodium nitroprusside (SNP; 1 x 10(9)-1 x 10(4)m), constr

256 -N-acetylpenicillamine (SNAP; 50 microM) and sodium nitroprusside (SNP; 100 microM) did not change th

257 In eight subjects increasing doses of sodium nitroprusside (SNP; 8.4 x 10(-6)-8.4 x 10(-3)m) w

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

259 ercise (5% maximum voluntary contraction) or sodium nitroprusside (SNP; endothelium-independent dilat

260 gulation of Ca(2+) channels by exogenous NO (sodium nitroprusside [SNP], 100 nmol/L) and cGMP (8-brom

261 P), the endothelium-independent vasodilator (sodium nitroprusside, SNP), or potassium chloride (KCl)

262 r, L-NAME); low-dose NO infusion (1.0 microM sodium nitroprusside, SNP); adrenergic blockade (10 mM b

263 on capacity of vascular smooth muscle cells (sodium nitroprusside; SNP).

264 urthermore, CCTeta had no effect on basal or sodium nitroprusside-stimulated alphabeta(Cys-105) sGC,

265 Sodium nitroprusside stimulation of the cGMP-generating

266 ates cutaneous vasodilatation in response to sodium nitroprusside, suggesting that ET-1 diminishes th

267 The application of sodium nitroprusside to histamine-contracted media cause

268 formed by i.v. injection of phenylephrine or sodium nitroprusside to increase or decrease arterial bl

269 f the heart received infusion of intravenous sodium nitroprusside to reduce blood pressure and arteri

270 e report that 1) the ability of the NO donor sodium nitroprusside to reduce blood pressure is impaire

271 ylcholine and substance P) and -independent (sodium nitroprusside) vasodilators were measured in eigh

272 Sodium nitroprusside was administered to reduce blood pr

273 The nitric oxide (NO) donor sodium nitroprusside was injected intraperitoneally (2 m

274 of heart rate to transient hypotension with sodium nitroprusside was normalized by 66% compared with

275 R vessels to endothelium-independent agonist sodium nitroprusside was not altered, the endothelium-de

276 The response to sodium nitroprusside was not different between treatment

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

278 ites were locally heated to 43 degrees C and sodium nitroprusside was perfused to elicit maximal vaso

279 Maximal relaxation to sodium nitroprusside was similar in aorta from normal an

280 respectively, P=0.02), whereas DeltaCVR with sodium nitroprusside was similar in both groups (-55+/-2

281 rillatory action of both carbamylcholine and sodium nitroprusside was ultimately dependent on muscari

282 dilation to endothelium-independent NO donor sodium nitroprusside was unaffected after all time perio

283 e to the endothelium-independent vasodilator sodium nitroprusside was unaffected by AGE-Glu.

284 the endothelium-independent vasodilation to sodium nitroprusside was unaffected.

285 sels, whereas direct vessel relaxation using sodium nitroprusside was unaltered.

286 Sodium nitroprusside was used as an endothelium-independ

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

288 nylephrine or the fall in pressure evoked by sodium nitroprusside, was significantly attenuated in de

289 re infusion of acetylcholine, substance P or sodium nitroprusside were 25 +/- 4, 30 +/- 7 and 29 +/-

290 s and relaxation responses to bradykinin and sodium nitroprusside were assessed at days 5 and 10 post

291 responses to intrabrachial acetylcholine and sodium nitroprusside were assessed using venous occlusio

292 Acetylcholine and sodium nitroprusside were iontophoresed into the forearm

293 ubstance P, isoproterenol (isoprenaline) and sodium nitroprusside were measured by strain-gauge pleth

294 ntra-arterial infusions of acetylcholine and sodium nitroprusside were measured by strain-gauge pleth

295 itivity (P < 0.05) to the nitric oxide donor sodium nitroprusside were reduced in protein-restricted

296 s the dose-response curves to bradykinin and sodium nitroprusside were repeated with a coinfusion of

297 pothesis, vasorelaxation responses to BK and sodium nitroprusside were similar before and 219+/-37 da

298 uring vasoactive challenge (acetylcholine or sodium nitroprusside) were quantified in vivo in pigs by

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

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