ライフサイエンスコーパス: L-NMMA

1 L-NMMA (30 microM), a NO synthase inhibitor, blocked 5-H

2 L-NMMA (40 mg x kg(-1) given intravenously over a period

3 L-NMMA also dose-dependently increased NOS-derived (*)O

4 L-NMMA decreased basal forearm blood flow (from 2.35+/-0

5 L-NMMA decreased LPS-induced MIP-1 alpha protein release

6 L-NMMA decreased the stroke dimension to a greater exten

7 L-NMMA did not affect the response to sodium nitroprussi

8 L-NMMA during hypoxic exercise only blunted the compensa

9 L-NMMA enhanced +dP/dt responses similarly at 10 mg/kg (

10 L-NMMA had no significant effect on vasodilator response

11 L-NMMA inhibited acetylcholine-induced epicardial and mi

12 L-NMMA plus ketorolac did not impact total RH FBF before

13 L-NMMA produced sustained increases in systemic vascular

14 L-NMMA reduced blood flow by 25% and increased resistanc

15 L-NMMA reduced blood flow by 31.7+/-4.9% and percentage

16 L-NMMA reduced the blood flow response to acetylcholine

17 (L-NMMA slightly decreased albumin permeation in the reti

18 L-NMMA treatment decreased the histological evidence of

19 L-NMMA, glibenclamide, or 5-hydroxydecanoic acid adminis

20 L-NMMA-treated mice exhibited a slight reduction in vaso

21 32 ml, P = 0.001; LVC: control: 2.9 +/- 0.5; L-NMMA: 0.8 +/- 0.3 ml mmHg(-1), P < 0.001).

22 ve) by nearly 80% (LBF: control: 270 +/- 51; L-NMMA: 75 +/- 32 ml, P = 0.001; LVC: control: 2.9 +/- 0

23 1), P = 0.03) and LVC (control: 7.5 +/- 0.8; L-NMMA: 4.1 +/- 1.1 ml min(-1) mmHg(-1), P = 0.02) and d

24 e peak increase in LBF (control: 653 +/- 81; L-NMMA: 399 +/- 112 ml(-1) min(-1), P = 0.03) and LVC (c

25 osure to N(G)-monomethyl L-arginine acetate (L-NMMA), a nitric oxide synthase inhibitor, and Rp-8 CPT

26 After L-NMMA incubation, the decrease in slope was significant

27 ions with substance P or acetylcholine after L-NMMA were similar in patients with and without risk fa

28 LVEDP was elevated after L-NMMA and hemoglobin but reduced after sodium nitroprus

29 control after saline+PE, but enhanced after L-NMMA (P<0.001).

30 were the same, although they increased after L-NMMA and saline+PE (volume and pressor control for L-N

31 Increased resistance after L-NMMA in the presence of rHb1.1 indicated that rHb1.1 r

32 7 and P<0.001, respectively, versus room air L-NMMA responses).

33 Although L-NMMA did not alter the immediate increase (initial app

34 Although L-NMMA significantly decreased serum nitrite/nitrate lev

35 ic pressure dimension relationship, although L-NMMA shifted the relationship rightward (1.7+/-0.7 mm,

36 Acetylcholine and L-NMMA responses were significantly impaired (P=0.01 and

37 MA uptake studies demonstrated that ADMA and L-NMMA accumulate in endothelial cells with intracellula

38 tic activity was selective for free ADMA and L-NMMA and was incapable of hydrolyzing peptide incorpor

39 sured the dose-dependent effects of ADMA and L-NMMA on (*)O 2 (-) production from eNOS under conditio

40 fore, the dose-dependent effects of ADMA and L-NMMA on eNOS function were determined.

41 sured the dose-dependent effects of ADMA and L-NMMA on the rate and amount of O(2)(.) production from

42 ues of 356 and 154 nmols/mg/min for ADMA and L-NMMA, respectively.

43 and 1.1 microM were determined for ADMA and L-NMMA, respectively.

44 studies suggest, just as for l-arginine and L-NMMA, the binding of ADMA shifts the eNOS heme to the

45 However, control and L-NMMA cardiac index values were similar (p > .4), perha

46 Passive movement in control and L-NMMA trials evoked similar increases in heart rate, st

47 rformed: control; L-NMMA plus ketorolac; and L-NMMA plus ketorolac plus BaCl2 plus ouabain.

48 d Mphi apoptosis was inhibited by L-NAME and L-NMMA, it appears that morphine-induced Mphi apoptosis

49 Responses to nitroprusside and L-NMMA were not significantly different between smokers

50 by fluconazole and was reduced by L-NMMA and L-NMMA+fluconazole to a lesser extent than in controls.

51 FBF (-50+/-6%; P<0.05), whereas ouabain and L-NMMA plus ketorolac did not.

52 ursor for the synthesis of nitric oxide, and L-NMMA (NG-monomethyl-L-arginine), a nitric oxide syntha

53 fferential CO responses to phenylephrine and L-NMMA were primarily attributable to changes in preload

54 The results obtained with propranolol and L-NMMA suggest that beta-adrenergic mechanisms and local

55 was reversed by pretreatment with RpcGMP and L-NMMA.

56 Resting FBF decreased with TEA and L-NMMA in all subjects (P<0.001); however, the vasoconst

57 qual to the sum of those produced by TNF and L-NMMA given separately.

58 g, the cardiac-depressant effects of TNF and L-NMMA given together became equal to the sum of those p

59 at the cardiac-depressant effects of TNF and L-NMMA given together were significantly less than addit

60 be similar while suffusing with vehicle and L-NMMA (100 microM).

61 se (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA) (0.1 mmol/l).

62 nthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA) (3 mg kg(-1)) or increasing bolus doses of the n

63 N(omega)-monomethyl-L-arginine (L-NMMA) 10 mg/kg followed by 0.5, 1.0, or 4.0 mg/kg/hr),

64 th intracoronary N(G)-monomethyl-L-arginine (L-NMMA) 64 micromol/min for 5 minutes.

65 nthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA) abolished stimulated NO production and attenuate

66 NO synthase with N(G)-monomethyl-L-arginine (L-NMMA) affected neither the decline in PKCdelta activit

67 ynthase inhibitor N G-monomethyl-L-arginine (L-NMMA) after stellate block virtually eliminated all of

68 e effects of N(omega)-monomethyl-L-arginine (L-NMMA) and fluid loading on tumor necrosis factor (TNF)

69 (20 micromol l-1) N G-monomethyl-L-arginine (L-NMMA) and N G-nitro L-arginine (L-NNA) to the superfus

70 ynthase (NOS) with NG-monomethyl-L-arginine (L-NMMA) causes acute insulin resistance (IR), but the me

71 n both groups, but NG-monomethyl-L-arginine (L-NMMA) did not inhibit relaxations in rings from transg

72 O synthesis with N(G)-monomethyl-L-arginine (L-NMMA) followed by forearm exercise stress.

73 pressor doses of N(G)-monomethyl-L-arginine (L-NMMA) in C57B6 and Tie-2/green fluorescent protein mou

74 rial infusion of N(G)-monomethyl-L-arginine (L-NMMA) increased iliac PWV significantly, by 3+/-2% (P<

75 loride (L-NAME) or NG-monomethyl-L-arginine (L-NMMA) reduced the increase in DAF-FM fluorescence obse

76 ine (ADMA) and N (G)-monomethyl- l-arginine (L-NMMA) regulate nitric oxide (NO) production from endot

77 inine (ADMA) and N(G)-monomethyl-L-arginine (L-NMMA) regulate nitric oxide (NO) production from neuro

78 ial dysfunction, N(G)-monomethyl-L-arginine (L-NMMA) was infused into the brachial arteries of 9 heal

79 cetylcholine and N(G)-monomethyl-L-arginine (L-NMMA) were used to assess stimulated and basal endothe

80 -1) x min(-1) or N(G)-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of nitric oxide synthas

81 is in rats with N:(G)-monomethyl-L-arginine (L-NMMA), a competitive nonspecific inhibitor of both con

82 x-/-) mice using N(G)-monomethyl-L-arginine (L-NMMA), a large proportion of these mice eventually suc

83 etreatment with N:(G)-monomethyl-L-arginine (L-NMMA), a nitric oxide synthase (NOS) inhibitor; BQ-788

84 ed the effect of N(G)-monomethyl-L-arginine (L-NMMA), a nonspecific NOS inhibitor, in three models of

85 hylarginine (ADMA) and NG-methyl-L-arginine (L-NMMA), are released in cells upon protein degradation

86 nthase activity, N(G)-monomethyl-L-arginine (L-NMMA), or, as a control, with PBS or D-NMMA.

87 ial infusions of N(G)-monomethyl-l-arginine (L-NMMA), TEA, fluconazole, and their combination.

88 2 (n=9), 3 mg/kg N(G)-monomethyl-L-arginine (L-NMMA), which crosses the blood-brain barrier and inhib

89 he LBF response to NG-monomethyl-L-arginine (L-NMMA), which is an inhibitor of NO synthase.

90 g acetylcholine and N-monomethyl-L-arginine (L-NMMA), with sodium nitroprusside as a control vasodila

91 ministration of N:(G)-monomethyl-L-arginine (L-NMMA).

92 l application of N(G)-monomethyl-L-arginine (L-NMMA).

93 synthase inhibitor N-monomethyl-L-arginine (L-NMMA).

94 rial infusion of N(G)-monomethyl-L-arginine (L-NMMA).

95 the NO-inhibitor, NG-monomethyl-L-arginine (L-NMMA).

96 6.6 mg.kg.h-1 N omega-monomethyl-L-arginine (L-NMMA).

97 troprusside, and N(G)-monomethyl-L-arginine (L-NMMA).

98 nthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA).

99 O inhibition with NG-mono-methyl-L-arginine (L-NMMA).

100 synthase inhibitor NG-monomethyl-L-arginine (L-NMMA).

101 synthase inhibitor NG-monomethyl-L-arginine (L-NMMA); and nitroprusside was used to assess sensitivit

102 the presence of N(G)-monomethyl-L-arginine (L-NMMA, 10 micromol/L; n=10) or free hemoglobin (1 micro

103 yclooxygenase), or NG-monomethyl-L-arginine (L-NMMA, 100 mg/kg, to inhibit NO synthase) were then inf

104 ase inhibitor L-N:(G)-monomethyl-L-arginine (L-NMMA, 4 micromol/min intra-arterially), and (3) the cy

105 sion of saline and NG-monomethyl-L-arginine (L-NMMA, 4 mumol.min-1), an inhibitor of nitric oxide syn

106 he NOS inhibitor N(G)-monomethyl-L-arginine (L-NMMA, 5 mg/min).

107 ed with a 1 mmol/L NG-monomethyl-L-arginine (L-NMMA, a NO synthase inhibitor).

108 NO production) and NG-monomethyl-L-arginine (L-NMMA, an inhibitor of NO production).

109 nthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA; 100 microM) significantly attenuated the VEGF-in

110 ynthase inhibitors NG-monomethyl-L-arginine (L-NMMA; 100 micromol/l) or 7-nitroindazole (1 mmol/l).

111 inhibition with N(G)-monomethyl-L-arginine (L-NMMA; 20 mg/kg) had no effect on basal contractility o

112 inhibition with N(G)-monomethyl-L-arginine (L-NMMA; 25 micromol/min) on basal LV function and the re

113 of NO synthesis by NG-monomethyl-L-arginine (L-NMMA; 4 micromol/min).

114 de synthase (NOS), NG-monomethyl-L-arginine (L-NMMA; 50 micromoles/kg body weight infused simultaneou

115 after i.v. infusion of NG-methyl-L-arginine (L-NMMA; a nitric oxide synthase inhibitor), or L-NMMA fo

116 OS inhibition with NG-monomethyl-L-arginine (L-NMMA; n = 6) or NG-nitro-L-arginine methyl ester (L-NA

117 in the presence of L-NG-monomethyl arginine (L-NMMA) (NOS inhibitor) but not of D-NG-monomethyl argin

118 nthase inhibitor L-N(G)-monomethyl arginine (L-NMMA) and endothelin-1 were also determined.

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

120 thylarginine (ADMA) and monomethyl arginine (L-NMMA) are endogenously produced amino acids that inhib

121 letely inhibited by L-N-monomethyl arginine (L-NMMA), a specific inhibitor of the L-arginine:NO pathw

122 nhibitors of iNOS, L-NG-monomethyl arginine (L-NMMA), and L-arginine-methyl ester (L-NAME) had little

123 e NOS inhibitor, L-N(G)-monomethyl arginine (L-NMMA, 1 mM).

124 and NO synthase (N(G)-monomethyl-l-arginine [L-NMMA]).

125 After discontinuing L-arginine, L-NMMA (1.0 microM) was microdialyzed into the RVLM for

126 and nitric oxide (NG-monomethyl-L-arginine, L-NMMA) regulation of blood flow.

127 hase inhibition (N(G)-monomethyl-L-arginine, L-NMMA).

128 nthase (NOS; via N(G)-monomethyl-L-arginine: L-NMMA) and cyclooxygenase (COX; via ketorolac).

129 nthase inhibition (NG-monomethyl-L-arginine; L-NMMA) under normoxic and normocapnic hypoxic (80% arte

130 oxide synthase (N(G)-monomethyl-L-arginine; L-NMMA; 10 and 100 microM).

131 fan and control subjects, and intra-arterial L-NMMA produced similar reductions in brachial artery di

132 MA produced constriction of pial arterioles, L-NMMA did not alter the permeability characteristics of

133 alues were similar (p > .4), perhaps because L-NMMA increased pulmonary artery occlusion pressure (p

134 performance than expected), possibly because L-NMMA augmented cardiac preload as shown by significant

135 Before L-NMMA administration, NOx concentrations and release of

136 significant difference in heart rate between L-NMMA and saline+PE.

137 trol (saline) conditions was similar between L-NMMA only (protocol 1) and combined L-NMMA-aminophylli

138 Both L-NMMA and ADMA are eliminated largely through active me

139 Both L-NMMA and TEA attenuated bradykinin-mediated vasodilati

140 Whereas both L-NMMA and L-NIL inhibited nitrite production by strepto

141 unaffected; IL-10 was augmented (123.4%) by L-NMMA.

142 ness to caffeine and Ca2+o were abolished by L-NMMA and AMT.

143 heating in controls (an effect abolished by L-NMMA) and, to a lesser extent, in patients, whereas, i

144 ed increases in RAR activity were blunted by L-NMMA (P = 0.006) but not by L-NMMA-L-arginine (P = 0.4

145 ficantly (both P<.01) and equally blunted by L-NMMA in both groups (maximum blood flow: 11+/-3 mL x m

146 choline-induced dilation was more blunted by L-NMMA than by CbTX+AP (-71% versus -44%, P:<0.002) and

147 P-evoked increases in RL were not changed by L-NMMA (P = 0.10) and were enhanced by L-NMMA-L-arginine

148 arterial blood pressure were not changed by L-NMMA or by L-NMMA-L-arginine.

149 tic shock (p = .01) and further decreased by L-NMMA (p = .02).

150 ed more in patients (an effect diminished by L-NMMA).

151 ed by L-NMMA (P = 0.10) and were enhanced by L-NMMA-L-arginine (P = 0.03).

152 onazole, L-NMMA, and, to a larger extent, by L-NMMA+fluconazole.

153 d by the percent decrease in flow induced by L-NMMA, was depressed in male compared with female patie

154 bachol-induced venodilation was inhibited by L-NMMA (48.9+/-6.2% reversal of maximal venodilation, P<

155 hat nitric oxide production was inhibited by L-NMMA in canine septic shock, but mortality and myocard

156 tics due to ascorbate were also inhibited by L-NMMA.

157 production is also specifically inhibited by L-NMMA.

158 milar in both groups and was not modified by L-NMMA.

159 ere blunted by L-NMMA (P = 0.006) but not by L-NMMA-L-arginine (P = 0.42).

160 od pressure were not changed by L-NMMA or by L-NMMA-L-arginine.

161 Heart rate was significantly reduced by L-NMMA (P<0.05) for control and VVS compared with baseli

162 t affected by fluconazole and was reduced by L-NMMA and L-NMMA+fluconazole to a lesser extent than in

163 ut and splanchnic blood flow were reduced by L-NMMA for control and VVS (P<0.05) compared with baseli

164 this anti-adrenergic effect was reversed by L-NMMA co-infusion (p < 0.05 vs. enalaprilat).

165 ion were unimpaired in VVS and unaffected by L-NMMA.

166 increases in LV dP/dt(max) were unaltered by L-NMMA.

167 P/dt(max) in these patients was unaltered by L-NMMA.

168 In patients with dilated cardiomyopathy, L-NMMA had no effect on baseline LV dP/dt(max) (from 131

169 intra-arterial saline (control) and combined L-NMMA-aminophylline (adenosine receptor antagonist) adm

170 etween L-NMMA only (protocol 1) and combined L-NMMA-aminophylline (protocol 2) at 10% (-17.5 +/- 3.7

171 In protocol 2, administration of combined L-NMMA-aminophylline reduced the DeltaFVC due to hypoxic

172 At higher concentrations, L-NMMA (500 microM) inhibited NO release but augmented P

173 llowing 3 RH trials were performed: control; L-NMMA plus ketorolac; and L-NMMA plus ketorolac plus Ba

174 In controls, L-NMMA significantly reduced basal LV dP/dt(max) (from 1

175 d to WT and untreated p47(phox-/-) controls, L-NMMA-treated p47(phox-/-) mice resolved their infectio

176 In normal conscious dogs, L-NMMA increased myocardial oxygen consumption (MVO2) wh

177 subjects inhaling NO, blood flow fell during L-NMMA infusion by only 10.9+/-7.3%, and the percentage

178 n, resistance was significantly lower during L-NMMA infusion, both at rest and during repetitive hand

179 in afterload (effective arterial elastance), L-NMMA increased preload (end-diastolic dimension) to a

180 iated dilatation was reduced by fluconazole, L-NMMA, and, to a larger extent, by L-NMMA+fluconazole.

181 nd saline+PE (volume and pressor control for L-NMMA).

182 On the other hand, L-NMMA blocked the response to dimaprit, but not that to

183 However, L-NMMA-treated p47(phox-/-) mice lost resistance to chro

184 hibitor L-N(G)-methylarginine hydrochloride (L-NMMA HC1 546C88) causes reductions in cardiac output (

185 on with L-N(G)-methylarginine hydrochloride (L-NMMA) on beta-adrenergic inotropy was assessed in cons

186 These results suggest that if L-NMMA has a beneficial effect on survival rates in sept

187 mposed arginine bolus were reduced by 28% in L-NMMA-infused rats compared with D-NMMA.

188 ratase-1 expression levels were decreased in L-NMMA-treated animals; this phenotype was absent in nit

189 ine-induced cell death because NOS inhibitor L-NMMA efficiently protected cells from apoptosis.

190 By contrast, the NOS inhibitor L-NMMA significantly reduced basal choroidal blood flow

191 duction with the NO synthase (NOS) inhibitor L-NMMA causes a significant increase in Tat-induced NF-k

192 or the nitric oxide synthase (NOS) inhibitor L-NMMA may alter the choroidal blood flow response durin

193 of inducible nitric oxide synthase inhibitor L-NMMA at concentrations that inhibit nitrite accumulati

194 oM), for 30 min, and after the NO inhibitor, L-NMMA (1.0 microM), for 30 min.

195 We find that an NOS inhibitor, L-NMMA, blocked regeneration of lymphatic vessels.

196 The NOS inhibitor, L-NMMA, blocked VEGF-induced vascular hyperpermeability

197 L-NMMA, n = 8) but not affected by 10 mg/kg L-NMMA (34+/-10%, P = NS; n = 8).

198 d this was augmented to 66+/-24% by 20 mg/kg L-NMMA (P = 0.04 versus without L-NMMA, n = 8) but not a

199 nges in group 3; and group 5 (n=6), 10 mg/kg L-NMMA infused into the heart transplant recipients.

200 both eNOS and nNOS; group 3 (n=13), 10 mg/kg L-NMMA; group 4 (n=8), phenylephrine titrated to simulat

201 malities were eliminated with fluid loading, L-NMMA had no beneficial effect on TNF-induced cardiac d

202 10(-)(4) M BQ-788 (P < 0.01) and 10(-)(3) M L-NMMA (P < 0.05).

203 demonstrating a 102% increase at 100 microM L-NMMA.

204 activity (preincubation of myocytes in 1 mM L-NMMA (N(G)-monomethyl-L-arginine) + 1 mM L-NNA (N(G)-n

205 L-arginine) for 2-3 h plus inclusion of 1 mM L-NMMA + 1 mM L-NNA in the patch pipette solution) produ

206 and N(G)-monomethyl-L-arginine monoacetate (L-NMMA), inhibitors of NO synthase, attenuated the morph

207 bitor, NG-monomethyl-L-arginine.monoacetate (L-NMMA), showed that NO released by the IgG-incubated IP

208 n the presence of L-N(G)-monomethylarginine (L-NMMA).

209 Tetracycline(s) and L-N-monomethylarginine (L-NMMA) (NO synthase inhibitor) showed an additive effec

210 Tilarginine (L-N(G)-monomethylarginine [L-NMMA]), 1-mg/kg bolus and 1-mg/kg per hour 5-hour infu

211 nitrite reductase activity, in RBCs L-NAME, L-NMMA, and L-arginine inhibited nitrite-derived NO prod

212 Neither L-NMMA nor epinephrine, individually or combined, signif

213 Neither L-NMMA nor phenylephrine affected the slope of the end-s

214 ut not of D-NG-monomethyl arginine (D-NMMA) (L-NMMA-inactive enantiomer).

215 e endoderm produced NO and inhibition of NO (L-NMMA) at this stage resulted in developmental arrest a

216 In the absence of L-NMMA, endothelium-independent vasodilation was not sig

217 cts of L-NMMA, indicating that the action of L-NMMA is specifically caused by inhibition of nitric ox

218 Addition of L-NMMA further augmented cytokine-induced PGE2 productio

219 Subsequent administration of L-NMMA (1.0 microM) into the CVLM for an additional 30 m

220 Oral administration of L-NMMA caused significant inhibition of choroidal neovas

221 In conclusion, ICV administration of L-NMMA causes hyperglycemia via the induction of defects

222 ICV administration of L-NMMA resulted in a 30% rise in the basal glucose level

223 clamps performed after ICV administration of L-NMMA were reduced by 22% compared with D-NMMA.

224 F response to intrafemoral administration of L-NMMA, an inhibitor of nitric oxide synthase, was also

225 ype groups before or after administration of L-NMMA.

226 s inhibited (>80%) by topical application of L-NMMA (10 microM).

227 Further, topical application of L-NMMA did not affect dilatation of the basilar artery i

228 Topical application of L-NMMA only partially inhibited dilatation of the basila

229 Although topical application of L-NMMA produced constriction of pial arterioles, L-NMMA

230 Subsequent application of L-NMMA significantly decreased GABA levels (from 0.47+/-

231 The coadministration of L-NMMA eliminated the vitamin C-related augmentation in

232 significantly inhibited during coinfusion of L-NMMA (P=0.03).

233 The concentration of L-NMMA for inhibition of MIP-1 alpha release was depende

234 tion by >/=85% with higher concentrations of L-NMMA shows 1) up-regulation of PGE2 production, 2) acc

235 However, there was no effect of L-NMMA on basal (P:=0.7) or bradykinin-stimulated tPA re

236 d abolished the beneficial preload effect of L-NMMA on cardiac performance.

237 od-brain barrier, we examined the effects of L-NMMA (10 and 100 microM).

238 xide precursor which reverses the effects of L-NMMA).

239 arginine reversed the constrictor effects of L-NMMA, indicating that the action of L-NMMA is specific

240 , 60 minutes) mimicked inhibitory effects of L-NMMA.

241 Infusion of L-NMMA alone caused venoconstriction (9.1+/-6.4% increas

242 Infusion of L-NMMA alone decreased vascular conductance in choroid/s

243 Importantly, infusion of L-NMMA or acetylcholine distal to the common iliac arter

244 trained, and unstressed; all ICV infusion of L-NMMA or D-NMMA (control) were performed with artificia

245 During infusion of L-NMMA, HPV increased to 38 +/- 4%.

246 Injection of L-NMMA increased mean arterial pressure by 17 +/- 2 mmHg

247 A subsequent microdialysis of L-NMMA into the CVLM reversed the effects of L-arginine.

248 hibition was not observed in the presence of L-NMMA or after endothelial removal but was prevented by

249 , epinephrine, in the absence or presence of L-NMMA, blunted recovery of cardiac index (p < .02) and

250 ase inhibition, demonstrated with our use of L-NMMA.

251 adult rat cardiomyocytes when either 3AB or L-NMMA were applied.

252 ects of sodium nitroprusside, but not ACH or L-NMMA, were reproduced in vitro.

253 NMMA; a nitric oxide synthase inhibitor), or L-NMMA followed by L-arginine (a nitric oxide precursor

254 lol, but neither phentolamine, yohimbine, or L-NMMA altered this response.

255 thase (NOS) inhibitors (L-NAME; 50 pmol) or (L-NMMA; 200 pmol) prevented the ANGII-induced baroreflex

256 ase, NO, and prostaglandins (BaCl2, ouabain, L-NMMA [N(G)-monomethyl-L-arginine] and ketorolac, respe

257 Phenylephrine, L-NMMA or placebo was administered on different study da

258 ethacin alone (P:=0.99) or indomethacin plus L-NMMA (P:=0.36) on bradykinin-stimulated tPA release.

259 saline treatment after rHb1.1 resuscitation, L-NMMA increased MAP and regional resistances in virtual

260 Saline, L-NMMA, or indomethacin treatment after resuscitation.

261 (G)-monomethyl-L-arginine, monoacetate salt (L-NMMA).

262 d approximately 50% by blocking NO synthase (L-NMMA) or K(+)(Ca) [charybdotoxin (CbTX)+apamin (AP)].

263 In contrast to tetracyclines, L-NMMA at low concentrations (< or = 100 microM) inhibit

264 We found that L-NMMA (1.0 microM) did not alter constrictor responses

265 Given that L-NMMA is a nonspecific inhibitor of NOS, the present st

266 alysis of fluorescence intensity showed that L-NMMA-treated animals exhibited lower fluorescence of M

267 atory cytokine, these data also suggest that L-NMMA acts as an anti-inflammatory agent by specificall

268 at seen with BQ123 but failed to augment the L-NMMA response.

269 Strikingly, the L-NMMA-mediated suppression of pneumonia occurred despit

270 onfidence interval, 3 to 40; P=0.02), and to L-NMMA by 10% (95% confidence interval, -1 to 23; P=0.07

271 that the greater fall in CO attributable to L-NMMA primarily reflects a difference in venoconstricti

272 sociated increase in vasoconstriction due to L-NMMA (-35+/-6% versus -18+/-4%; P<0.05).

273 timulated cells was unaltered on exposure to L-NMMA.

274 LBF in response to L-NMMA decreased by 17.3 +/- 2.4 and 9.0 +/- 1.4% in the

275 r degrees of vasoconstriction in response to L-NMMA in both groups, endothelin-1 caused a reduction i

276 1); however, the vasoconstrictor response to L-NMMA was greater (P=0.04) and to TEA was lower (P=0.04

277 elium-dependent vasoconstrictive response to L-NMMA was significantly improved only with nebivolol tr

278 LBF decrements in response to L-NMMA were 34.9+/-4.1% and 17.1+/-4.2% in women and men

279 esion molecule-1 and blood flow responses to L-NMMA and nitroprusside (r=0.53, P=0.004 and r=-0.66, P

280 than phenylephrine (9.6%+/-1.6%, p < .05 vs. L-NMMA).

281 When L-NMMA was added, there was no further reduction in the

282 tion, ADMA had no effect on O(2)(.), whereas L-NMMA increased O(2)(.) production almost 3-fold.

283 from a rate of 56 to 23 nmol/mg/min, whereas L-NMMA (0.1-100 microm) had no effect.

284 NP-stimulated 2-deoxyglucose uptake, whereas L-NMMA did not inhibit contraction-stimulated 2-deoxyglu

285 We tested whether L-NMMA-induced IR occurs via NOS blockade in the central

286 However, at the time at which L-NMMA maximally reduced substance P-induced RAR stimula

287 d IL-8 accumulation increased (p < .01) with L-NMMA.

288 Treatment of INS-1 cells with L-NMMA, an inhibitor of iNOS, provides the same degree o

289 Incubation of mouse peritoneal cells with L-NMMA, an inhibitor of nitric oxide synthase, or in med

290 l, followed in a subgroup by coinfusion with L-NMMA.

291 eolin-3 abundance positively correlated with L-NMMA augmentation of dobutamine inotropic responses in

292 with infection (p = .024) and decreased with L-NMMA (p = .004, all doses combined).

293 Infusion with L-NMMA before enalaprilat in patients with DCM (n = 5) p

294 be relieved by systemic NOS inhibition with L-NMMA.

295 ypoxic exercise was substantially lower with L-NMMA administration compared to saline (control; P < 0

296 of circulating adrenaline was observed with L-NMMA.

297 nd systemic treatment of arthritic rats with L-NMMA ablated synovitis, surprisingly L-NIL did not med

298 1) x 100 g tissue(-1), P<0.01) was seen with L-NMMA.

299 ilation declined more with CbTX+AP than with L-NMMA (-66% versus -46%, P:=0.03) and was fully blocked

300 by 20 mg/kg L-NMMA (P = 0.04 versus without L-NMMA, n = 8) but not affected by 10 mg/kg L-NMMA (34+/