ライフサイエンスコーパス: captopril

1 steine, glutathione, N-acetylcysteamine, and captopril.

2 ts and their prevention by the ACE inhibitor captopril.

3 nificantly increased by MI and normalized by captopril.

4 chelators and the metalloprotease inhibitor captopril.

5 s are valuable auxiliaries to agents such as captopril.

6 cantly reduced by 12% when the HTRs received captopril.

7 ACE2 is not inhibited by lisinopril or captopril.

8 xpected lower mortality than that found with captopril.

9 ngiotensin-converting enzyme inhibition with captopril.

10 ta inhibitor ruboxistaurin, or ACE inhibitor captopril.

11 and inulin clearances and their response to captopril.

12 but significantly restored by candesartan or captopril.

13 Captopril (0.5mg/kg/d SC) was given from P7 (post natal

14 /min), EXP3174 (0.1 mg/kg + 0.01 mg/kg/min), captopril (1 mg/kg + 0.5 mg/kg/h) or vehicle were infuse

15 Captopril (1 microM) inhibited the biosynthesis of angio

16 The ACE inhibitor captopril (1 micromol/L) also selectively reduced tdP/dt

17 er, angiotensin-converting enzyme inhibitor, captopril (10(-5) mol/l) augmented relaxations to angiot

18 ctivity significantly (P<0.01) compared with captopril (13% versus 61%).

19 ich one group was subsequently maintained on captopril (2 g l(-1))-containing drinking water, and at

20 arge myocardial infarction were treated with captopril (2 g/liter drinking water, n = 87) or losartan

21 c suppression of the RAA axis with high-dose captopril (225 mg/day) returned HTRs to a normovolemic s

22 fter four months, the same subjects received captopril (225 mg/day), and the protocol was repeated.

23 rs old) both before and after treatment with captopril (225 mg/day).

24 years) both before and after treatment with captopril (225 mg/day).

25 Six additional subjects received captopril 25 mg as a low-sodium comparison and also rece

26 injection of streptozotocin and treated with captopril (25 mg/kg body weight per day) or atenolol (10

27 th valsartan (4909 patients), valsartan plus captopril (4885 patients), or captopril (4909 patients).

28 valsartan plus captopril (4885 patients), or captopril (4909 patients).

29 beginning 3 months after banding with either captopril (5 mg x kg(-1) x d(-1)) or vehicle added to th

30 Administration of captopril (5 mg/L in the water) significantly reduced ne

31 50 mg PO TID, or valsartan 80 mg PO BID plus captopril 50 mg PO TID between 1 and 10 days after MI.

32 ndomized to receive valsartan 160 mg PO BID, captopril 50 mg PO TID, or valsartan 80 mg PO BID plus c

33 74, 2/8 (25%; p < 0.05 vs. vehicle control); captopril, 7/10 (70%).

34 (-1) x 1.73 m(-2)) and exceeded responses to captopril (92+/-20 mL x min(-1) x 1.73 m(-2); P<0.01).

35 muM, which is over 300-fold more potent than captopril, a known NDM-1 inhibitor.

36 nge in parenchymal MTT (post-captopril - pre-captopril) accuracy was 55%-61% and was not significantl

37 Both antioxidant therapy and captopril administration alleviated oxidative stress (as

38 the SHR treated before cardiac dysfunction, captopril administration attenuated hypertrophy and prev

39 Furthermore, captopril administration to sham-operated rats significa

40 In addition, the acute effect of oral captopril administration was completely abolished by pre

41 with anticoagulants, thrombolytic agents, or captopril affect long-term rates of stroke.

42 Captopril alone (1.78 +/- 0.31%) and with losartan (1.13

43 hemodynamic, renal, and endocrine effects of captopril alone (25 mg), captopril plus icatibant (100 m

44 V ejection fraction to a greater extent than captopril alone.

45 mm Hg, as compared with 14.0+/-1.0 mm Hg for captopril alone; P=0.001), in such a way that the decrea

46 ith 2.0+/-0.7 ng per milliliter per hour for captopril alone; P=0.007).

47 Captopril also completely abrogated renin stimulation in

48 These results indicate that captopril ameliorates experimental autoimmune myocarditi

49 Captopril ameliorates the myocarditis associated with ac

50 Pretreatment of the SFO with either captopril, an ANG converting enzyme inhibitor, or losart

51 p110delta was attenuated in SHR treated with captopril, an angiotensin (Ang)-converting enzyme inhibi

52 hen renin-injected rats were pretreated with captopril, an angiotensin converting enzyme inhibitor, d

53 Chronic administration of captopril, an angiotensin-converting enzyme inhibitor, b

54 Captopril, an angiotensin-converting enzyme inhibitor, i

55 Captopril, an angiotensin-converting enzyme inhibitor, i

56 lderly heart-failure patients, compared with captopril, an angiotensin-converting-enzyme (ACE) inhibi

57 one of two chemical inhibitors of MMP (MMPi; captopril and a chemically modified tetracycline) and re

58 be made using the alternative ACE inhibitors captopril and enalaprilat.

59 onstrated that two known NDM-1 inhibitors, L-captopril and ethylenediaminetetraacetic acid (EDTA), in

60 losartan was generally better tolerated than captopril and fewer patients discontinued losartan thera

61 Two inhibitors, captopril and fosinopril (a pro-drug ester of fosinopril

62 The combination of captopril and infection may have impaired renal function

63 otocin-induced diabetic rats was reversed by captopril and islet cell transplantation.

64 Similarly, captopril and lisinopril significantly inhibited intrace

65 o determine the effect of the RAS inhibitors captopril and losartan on acute liver damage and inflamm

66 the comparative effects of pretreatment with captopril and losartan on myocardial infarct size and ar

67 In contrast, both captopril and olmesartan significantly improved cardiac

68 tor phosphoramidon and to -7.3 +/- 0.20 with captopril and phosphoramidon combined.

69 mixture of peptidase inhibitors (amastatin, captopril and phosphoramidon) onto the lumbar spinal cor

70 Residual ACE activity was equivalent for the captopril and quinaprilat groups in plasma (42.54+/-0.03

71 The ACEI captopril and quinaprilate and the ARB candesartan signi

72 mined occurred at a similar frequency in the captopril and valsartan groups.

73 chemia/reperfusion with the use of an ACE-I (captopril) and an angiotensin II type 1 receptor blocker

74 es (amastatin), dipeptidyl carboxypeptidase (captopril), and neutral endopeptidase (phosphoramidon) d

75 4+/-4% before placebo, after placebo, before captopril, and after captopril, respectively.

76 +/-11% before placebo, after placebo, before captopril, and after captopril, respectively.

77 eceptor blocker valsartan, the ACE inhibitor captopril, and the combination of the two on mortality i

78 ngiotensin-converting enzyme (ACE) inhibitor captopril; and 3) increased ACE activity.

79 inas and cultured retinal endothelial cells, captopril at a concentration of 2 mM significantly inhib

80 Captopril attenuated diastolic LV dilatation at 2 years

81 The ACE-inhibitor captopril augmented relaxations similarly in both groups

82 r of therapy because changes in LV size with captopril beyond 1 year were similar to those with place

83 deteriorating function that is unaffected by captopril beyond 1 year.

84 cysteine, dithiothreitol, N-acetylcysteine, captopril, bovine and human serum albumins, and hydrogen

85 not alter the renal hemodynamic response to captopril, but it significantly altered the change in pl

86 rotected by phosphoramidon plus amastatin or captopril, but not by amastatin plus captopril or by pho

87 tors of AC reduced the stimulatory effect of captopril by 70% to 80%.

88 f known NDM-1 inhibitors, including L- and D-captopril by monitoring the changing chemical environmen

89 the angiotensin-converting enzyme inhibitor captopril (cap) (2.5 mM, 0.1 ml/min, 60 min) in six anes

90 5 micromol/L, n=12), Ang I+the ACE inhibitor captopril (cap) (2.5 mmol/L, n=4), Ang I+the chymase inh

91 the angiotensin-converting enzyme inhibitor captopril (CAP) were examined in wild-type (WT) or T26 m

92 the angiotensin-converting enzyme inhibitor, captopril (CAP).

93 the angiotensin-converting enzyme inhibitor captopril (Cap; 5 mg (kg bw)(-1)).

94 the angiotensin-converting enzyme inhibitor, captopril (Cap; 5 mg/kg, bw).

95 ion was preceded by treatment with a dose of Captopril, CAP, (an angiotensin-converting enzyme (ACE)

96 ed by an intravenous saline infusion test or captopril challenge test and subtype differentiation was

97 ensive drugs: hydrochlorothiazide, atenolol, captopril, clonidine, diltiazem (sustained release), or

98 ndomly allocated to treatment with atenolol, captopril, clonidine, diltiazem, hydrochlorothiazide, or

99 ndomly allocated to treatment with atenolol, captopril, clonidine, diltiazem, hydrochlorothiazide, or

100 Captopril completely reversed hypertension in mice perin

101 lsartan, either alone or in combination with captopril, could attenuate progressive LV enlargement or

102 es (DSOs) derived from glutathione (GSH) and captopril (CPSH) were synthesized by iron- or methyltrio

103 ave previously shown in an animal model that captopril (Cpt) reduced LV hypertrophy and protected LV

104 The captopril detections using both inhibition ways are very

105 ed methods have been successfully applied in captopril determination in spiked human serum and pharma

106 Captopril did not affect overall mortality but did delay

107 Patients who received captopril did not demonstrate more WRF than patients who

108 Interestingly, captopril did not directly affect Ag-specific T cell res

109 and atrial natriuretic peptide levels after captopril did not reach statistical significance.

110 osin-immunized, untreated mice, injection of captopril directly into the test site also suppressed my

111 (GS-DSDO) (IC50, approximately 30 microM) > captopril disulfide S-dioxide (CPS-DSDO) (IC50, approxim

112 utathione disulfide S-monoxide (GS-DSMO) and captopril disulfide S-monoxide (CPS-DSMO).

113 Increasing the captopril dose also led to a decrease in inflammation.

114 d diuretic agents; they were progressed to a captopril dose of 75 mg three times per day over 14 days

115 Captopril dramatically reduced the incidence and severit

116 Pups treated with captopril during hyperoxia had a lower median retinopath

117 The pups treated with captopril during hyperoxia had significant reduction in

118 Losartan, EXP3174 and captopril elevated plasma renin activities and comparabl

119 myocardium, kininogen (10 micrograms/mL) and captopril, enalaprilat, or ramiprilat (10(-4) mol/L) red

120 10 micrograms/mL) and three ACE inhibitors (captopril, enalaprilat, or ramiprilat; 10(-8) mol/L) inc

121 in renin production, rats were treated with captopril for one week with or without the specific COX-

122 n; and 51%, 83%, and 100%, respectively, for captopril for patients with baseline DBP of 95-99 mm Hg)

123 (for AT(2)), A-779 [for angiotensin-(1-7)], captopril (for angiotensin-converting enzyme), and amast

124 ACE inhibitors (captopril, fosinopril and fosinoprilat) and two peptides

125 ), angiotensin converting enzyme inhibitors (captopril, fosinopril, ramipril), and angiotensin recept

126 ion of the angiotensin converting inhibitor, captopril, further increased COX-2 mRNA and renal cortic

127 -and-captopril group and 958 patients in the captopril group (hazard ratio in the valsartan group as

128 ed with HR 1.33 (95% CI 0.81 to 2.21) in the captopril group (P = 0.49 for interaction).

129 ed, as did 941 patients in the valsartan-and-captopril group and 958 patients in the captopril group

130 1; P=0.98; hazard ratio in the valsartan-and-captopril group as compared with the captopril group, 0.

131 The valsartan-and-captopril group had the most drug-related adverse events

132 ted as having a fatal or non-fatal MI in the captopril group was 559 (total investigator reported eve

133 e comparison of the valsartan group with the captopril group was within the prespecified margin for n

134 tan-and-captopril group as compared with the captopril group, 0.98; 97.5 percent confidence interval,

135 in the valsartan group as compared with the captopril group, 1.00; 97.5 percent confidence interval,

136 se group, middle dose group, low dose group, captopril group, and control group.

137 nd taste disturbance were more common in the captopril group.

138 n in sham controls but were normal in the MI+captopril group.

139 ntinued due to cough compared with 14 in the captopril group.

140 (6.4%) patients with WRF in the placebo and captopril groups had no significant association between

141 3 and 104 +/- 3 mm Hg in the isradipine and captopril groups, respectively) and GFR was unchanged (d

142 d +1 +/- 3 ml/min/1.73 in the isradipine and captopril groups, respectively; P = NS).

143 the angiotensin-converting enzyme inhibitor captopril had an additive therapeutic benefit in control

144 Within 24 h captopril had killed >90% of the early instars of both s

145 ction, whereas administration of losartan or captopril had no effect.

146 Hence, captopril had no significant effect on the response to [

147 The use of thrombolytic agents and captopril had no significant effect on the risk of strok

148 with rats with untreated MI, rats receiving captopril had similar LV diastolic dimensions (10.5 +/-

149 stablished generic drugs such as digoxin and captopril have seen sharp and rapid increases.

150 Losartan and captopril have similar cardiovascular protective effects

151 giotensin converting enzyme (ACE) inhibitor, captopril (HC experiment), and normoxia alone with capto

152 ents with adequate blood pressure control on captopril, hydrochlorothiazide, and atenolol show a redu

153 nvestigated and compared with the effects of captopril in 31 African Americans with NIDDM and protein

154 d relative hypoxic recovery and modulated by captopril in a mouse model of OIR.

155 dies and no animal studies on the effects of captopril in CHD.

156 ncentration and the renovascular response to captopril in diabetes supports the hypothesis of a direc

157 C was given 40 mg/kg body weight per day of captopril in drinking water; and group L was given 40 mg

158 ata validate recent nonrandomized studies of captopril in HIV-infected patients, and suggest that an

159 A randomized placebo-controlled trial of captopril in HIVAN may be warranted.

160 y to confirm whether losartan is superior to captopril in improving survival and is better tolerated.

161 pril, the ELITE study compared losartan with captopril in older heart-failure patients.

162 Valsartan is as effective as captopril in patients who are at high risk for cardiovas

163 ma prorenin and the renovascular response to captopril in patients with diabetes (P < 0.01) but not i

164 ngiotensin-converting enzyme (ACE) inhibitor captopril in streptozotocin (STZ)-diabetic male Wistar r

165 60 pM, approximately 3-fold more active than captopril in the same assay.

166 geneic cardiac myosin, were given 75 mg/L of captopril in their drinking water.

167 Combining valsartan with captopril increased the rate of adverse events without i

168 an angiotensin-converting enzyme inhibitor (captopril) increased the vascular permeability.

169 internalization, and phosphoramidon, but not captopril, increased this effect, indicating that the ef

170 inhibition constant, K(i), for CdBcII with l-captopril indicates that pK(a1) = 8.7 +/- 0.1 correspond

171 aortas but was attenuated by candesartan or captopril, indicating that NOX remains active in nonendo

172 Interestingly, increasing the dose of captopril induced mortality in infected mice in a dose-d

173 These data indicate that the captopril-induced inhibition of glucose accumulation obs

174 ril (HC experiment), and normoxia alone with captopril infusion (NC experiment).

175 arameters and plasma [AII] were unaltered by captopril infusion, apart from a fall in MAP (NC experim

176 Captopril inhibited TGF-beta and collagen synthesis and

177 Treatment of rats with captopril inhibited the diabetes-induced accumulation of

178 r reduction of more than 70%, is present and captopril is administered.

179 ngiotensin-converting enzyme inhibitor drug, captopril, is presented.

180 FSDs (N-acetyl-L-cysteine, D-penicillamine, captopril, L-cysteine, or reduced glutathione] generate

181 Sodium depletion and captopril led to activation and differentiation of these

182 but not by classical ACE inhibitors such as captopril, lisinopril, or enalaprilat.

183 type 1 blocker candesartan or ACE inhibitor captopril markedly attenuated eNOS-derived O(2)*(-) and

184 icantly attenuated the hypotensive effect of captopril (maximal decrease in mean arterial pressure fo

185 2.9; 95% confidence limits, -65.5, -20.2 g), captopril (mean, -38.7; 95% confidence limits, -61.0, -1

186 hortening (16 +/- 2% vs. 9 +/- 1%, p < 0.05 [captopril MI vs. untreated MI]) and unchanged posterior

187 s preliminary experience in an animal model, captopril MR renography provided data consistent with ex

188 randomized to receive isradipine (N = 16) or captopril (N = 15); doses were adjusted to maintain simi

189 an (n = 352) titrated to 50 mg once daily or captopril (n = 370) titrated to 50 mg three times daily,

190 an (n=1,578) titrated to 50 mg once daily or captopril (n=1,574) titrated to 50 mg three times daily.

191 terial injection (n=6), quinaprilat (n=8) or captopril (n=7) administered as a daily subcutaneous inj

192 y, angiotensin-converting enzyme inhibition (captopril) normalized blood pressure and was associated

193 Pharmacological regression of LVH with captopril normalizes the in vivo and in vitro electrophy

194 rial, evaluating the effects of losartan and captopril on mortality and morbidity in a larger number

195 We investigated the effects of captopril on myocarditis and the host immune response to

196 We investigated the effect of captopril on myosin-induced experimental autoimmune myoc

197 the angiotensin-converting enzyme inhibitor captopril on wound healing in diabetic and aged mice wit

198 an angiotensin converting enzyme inhibitor, captopril, on oxygen-induced retinopathy (OIR) in the mo

199 atin or captopril, but not by amastatin plus captopril or by phosphoramidon alone, indicating that re

200 When hypertension was reduced using captopril or candesartan, retinal KDR expression returne

201 12 weeks after MI, respectively; 8 received captopril or captopril with losartan up to 4 weeks after

202 rise in [AII] during hypoxia was blocked by captopril or L-NAME infusion.

203 and treated with different concentrations of captopril or lisinopril for 5 days.

204 The effect of captopril or losartan (100 or 5 mg/kg intragastrically,

205 inducing diabetes, but treatment with either captopril or losartan prevented these effects.

206 Captopril or losartan treatment showed profound protecti

207 ter a 6.25-mg oral dose of the ACE inhibitor captopril or matching placebo.

208 GF and superior to that observed with either captopril or no drug (controls).

209 Rats were randomized to receive captopril or no treatment 1 day after MI.

210 mean arterial pressure; sex; treatment arm (captopril or placebo); smoking history; history of prior

211 6 d (average 11 d) after acute MI to receive captopril or placebo; those with a serum creatinine of >

212 s greater with hydrochlorothiazide than with captopril or prazosin.

213 ther studies, angiotensin-converting enzyme (captopril) or renin (CP-71362-14) was inhibited.

214 ol, angiotensin converting enzyme inhibitor, captopril, or placebo for 2 wks.

215 Valsartan, captopril, or the combination had comparable effects on

216 ssigned to receive treatment with valsartan, captopril, or the combination; follow-up continued for u

217 uced significantly only after treatment with captopril (P=0.002).

218 for adverse experiences (12.2% vs 20.8% for captopril, p = 0.002).

219 opril, p = 0.651 (0.965); combination versus captopril, p = 0.187 (0.350).

220 ) in the combination group; valsartan versus captopril, p = 0.651 (0.965); combination versus captopr

221 Captopril partially or completely inhibited changes in 1

222 ded in 9.4% of the losartan and 13.2% of the captopril patients (risk reduction 32% [95% CI -4% to +

223 VN might contribute to the overall effect of captopril, perhaps attributable to a consequent decrease

224 Captopril pharmacologically suppressed (p<0.05) supine r

225 ndocrine effects of captopril alone (25 mg), captopril plus icatibant (100 microg per kilogram of bod

226 n blood pressure after the administration of captopril plus icatibant was similar to that after the a

227 captopril, valsartan, or the combination of captopril plus valsartan resulted in similar changes in

228 Change in parenchymal MTT (post-captopril - pre-captopril) accuracy was 55%-61% and was

229 With the same captopril pretreatment, both Fos- and Egr-1-ir in the SF

230 bition of ACE with a widely prescribed drug, captopril, promoted the accumulation of cell-derived Abe

231 n-converting-enzyme (ACE) inhibitors such as captopril reduce mortality and cardiovascular morbidity

232 The ACE inhibitor captopril reduced Ang II levels in the media by 90% in t

233 Treatment of mice with metoprolol and captopril reduced DCM in Ca(v)1.2(I1624E) hearts at day

234 s 6 months, respectively, P < 0.05), whereas captopril reduced proteinuria by 30% after 6 months (2.8

235 nthesis in unoperated rats with 100 mg/kg of captopril reduced water intake only during the initial 1

236 EXP3174, but not losartan nor captopril, reduced the incidence of lethal ischemic vent

237 It was concluded that over 6 months, captopril reduces and isradipine increases proteinuria i

238 Captopril reduces retinal neovascularization in a mouse

239 opportunity to correlate the results of the captopril renogram with the renal artery angiograms in t

240 Systemic hypotension on captopril renograms results in preserved uptake of both

241 Captopril renography (CR) has been established in the pa

242 Most patients with these findings on captopril renography do not receive renal artery angiogr

243 Captopril renography had an estimated sensitivity of 78.

244 ystemic hypotensive response pattern seen on captopril renography is a distinctive pattern that does

245 A characteristic pattern seen on captopril renography is described that is due to systemi

246 Parenchymal MTT analysis of DTPA captopril renography is not more accurate and offers no

247 We used captopril renography to screen for renovascular disease.

248 The estimated positive predictive value of captopril renography was 89.7% and the negative predicti

249 Captopril renography was performed with a glomerular fil

250 riamine pentaacetic acid (DTPA) baseline and captopril renography, one (n = 43) with demographically

251 ith systemic hypotensive response pattern on captopril renography.

252 ith systemic hypotensive response pattern on captopril renography.

253 , after placebo, before captopril, and after captopril, respectively.

254 , after placebo, before captopril, and after captopril, respectively.

255 Before captopril, saline infusion suppressed the RAAS in LTRs b

256 bited activity, which can exceed activity of captopril-sensitive angiotensin-converting enzyme.

257 Both propranolol and captopril significantly decreased the duration of ventri

258 In the phase 2 study, both propranolol and captopril significantly increased the threshold of ventr

259 After captopril, sodium elimination was comparable in the live

260 Captopril specifically interfered with cell-mediated imm

261 Captopril, started 3 months after banding, caused regres

262 Proposed renal hemodynamic mechanisms of captopril suggest that quantitation of renographic reten

263 The effects of Ang1-9 were not inhibited by captopril, supporting previous evidence that Ang1-9 acts

264 s were similar for all modalities except the captopril test, which had a significantly lower sensitiv

265 In CSD, but not intact, fetuses infused with captopril the rise in MAP was absent, and the fall in FB

266 nsin-converting-enzyme (ACE) inhibition with captopril, the ELITE study compared losartan with captop

267 prazosin for younger black men, from 50% for captopril to 97% for diltiazem for older black men, from

268 Addition of captopril to the tissue bath during in vitro electrophys

269 the angiotensin-converting enzyme inhibitor captopril, to -6.33 +/- 0.19 with the neutral endopeptid

270 the angiotensin-converting enzyme inhibitor captopril, to block endogenous angiotensin formation.

271 giotensin converting enzyme (ACE) inhibitor, captopril, to evaluate sensitivity to amelioration of DD

272 a 6.2-fold suppression in ET-1 expression in captopril-treated animals when compared with the oxygen

273 etic at the ages of 7, 10 and 13 weeks and a captopril-treated group of animals made diabetic at the

274 trols and antioxidant (lazaroid)-treated and captopril-treated rats with CRF.

275 Captopril-treated, OVA-immunized mice also exhibited a d

276 rats (WKY) were assigned to no treatment or captopril treatment (2 g/L in drinking water) begun at a

277 on was less frequent with losartan than with captopril treatment (22.2% vs 29.7%).

278 iveness because neither in vivo nor in vitro captopril treatment affected the proliferation, IFN-gamm

279 Captopril treatment begun after cardiac function was imp

280 oups diabetic from 7 weeks demonstrated that captopril treatment relieved the alterations in critical

281 In an additional group, captopril treatment was begun when SHR developed heart f

282 Captopril treatment, which was started immediately after

283 ngiotensin-converting enzyme (ACE) inhibitor captopril upon such chronic physiological changes were t

284 We compared the effects of captopril, valsartan, and their combination on atheroscl

285 Patients were randomly assigned to receive captopril, valsartan, or both.

286 Treatment with the ACE inhibitor captopril, valsartan, or the combination of captopril pl

287 Captopril was administered to improve the specificity.

288 In the male SHR, early treatment with captopril was associated with the most marked attenuatio

289 were best in low- and medium-renin profiles; captopril was best in medium- and high-renin profiles (l

290 Placebo or captopril was given in a double-blind, randomized fashio

291 despite this, the renal vascular response to captopril was much larger (82.9 +/- 11.5 versus 13.6 +/-

292 the therapeutic effects of the ACE inhibitor captopril, we used a model of Ang II-induced hypertensio

293 These effects of captopril were abolished by NMMA, implying mediation by

294 the angiotensin-converting enzyme inhibitor captopril were assessed in a canine model of recent myoc

295 of a long-acting ACE inhibitor or 150 mg of captopril were studied.

296 he MtDapE was insensitive to inhibition by L-captopril which we show is consistent with novel mycobac

297 or is used to inhibit tyrosinase activity by Captopril, which is generally used to treat congestive h

298 bound to the potent competitive inhibitor l-captopril, which reveals a unique binding mechanism.

299 er MI, respectively; 8 received captopril or captopril with losartan up to 4 weeks after MI.

300 fit was observed with losartan compared with captopril, with the lower mortality using losartan prima

301 he hypothesis that chronic ACE inhibition by captopril would prevent and possibly reverse impairment