ライフサイエンスコーパス: enalaprilat

1 ersion to AngII via ACE activity (blocked by enalaprilat).

2 giotensin-converting enzyme (ACE) inhibitor (enalaprilat).

3 reversed by L-NMMA co-infusion (p < 0.05 vs. enalaprilat).

4 /- 48.1) acquisition after administration of enalaprilat.

5 f sympathetic nerve activity was enhanced by enalaprilat.

6 the alternative ACE inhibitors captopril and enalaprilat.

7 aken before and after coadministration of IC enalaprilat.

8 usside, before and after ACE inhibition with enalaprilat.

9 inhibitors such as captopril, lisinopril, or enalaprilat.

10 from -10.1+/-1% to -1.4+/-2% (P<0.001) after enalaprilat.

11 from 82+/-7 to 90+/-8 mL/min (P=0.05) after enalaprilat.

12 ry infusions of low-dose bradykinin (BK) and enalaprilat.

13 27+/-4% (p < 0.001) remained unchanged after enalaprilat.

14 ure and in control subjects before and after enalaprilat (0.02 mg/kg body weight intravenously).

15 atropine (complete autonomic blockade), and enalaprilat (0.02 mg/kg, ACE blockade).

16 before and during intracoronary infusion of enalaprilat (0.2 mg/min) with and without the NOS inhibi

17 ration of propranolol (1.0 mg/kg, ATL only), enalaprilat (0.3 mg/kg, ATL only), caffeine (5.0 mg/kg,

18 during atrial pacing (baseline, 0.82+/-0.11; enalaprilat, 0.98+/-0.07; P<0.05).

19 uated (bradykinin: 0 +/- 0% to -13 +/- 0.9%; enalaprilat: -0.3 +/- 0.3% to -17 +/- 2.1%; P < 0.05), w

20 (bradykinin: -2.5 +/- 0.9% to -21 +/- 1.5%; enalaprilat: -0.7 +/- 0.5% to -26 +/- 1.2%; amlodipine:

21 ere constructed for Ang I in the presence of enalaprilat 1 micromol/L, chymostatin 10 micromol/L, or

22 Moreover, enalaprilat (1 mumol/L) completely and immediately resto

23 In CHO-15AB cells, enalaprilat (1 mumol/L) increased the total number of lo

24 Enalaprilat (1.25 mg IV) improved transmural distributio

25 rdial ratio) at rest (baseline, 0.91+/-0.11; enalaprilat, 1.02+/-0.07 mL/min per g; P<0.05) and durin

26 (-8) M exogenous angiotensin II was added to enalaprilat (10(-4) M) in the luminal perfusate, fluid r

27 HR than WKY (SHR: bradykinin -13.9 +/- 1.9%, enalaprilat -15.3 +/- 1.6%, amlodipine -11.9 +/- 0.7%; W

28 .9 +/- 0.7%; WKY: bradykinin -22.8 +/- 1.0%, enalaprilat -24.1 +/- 2.0%, amlodipine -20.7 +/- 2.3%; P

29 g drugs: bradykinin (-34+/-3% vs. -24+/-5%), enalaprilat (-37+/-5% vs. -23+/-5%) and amlodipine (-43+

30 We measured the effect of intra-arterial enalaprilat (5 micro g/min) on forearm blood flow (FBF)

31 Enalaprilat (5 nmol to 1 mumol/L) potentiated the releas

32 to receive either an intracoronary bolus of enalaprilat (50 mug) or placebo before elective PCI.

33 .3 ng x min(-1) x 100 mL(-1), P=0.036 versus enalaprilat alone).

34 Enalaprilat also restored subendocardial coronary flow r

35 Patients pre-treated with enalaprilat also showed lower peak values (mean: 21.7 ng

36 Similarly, luminal 10(-4) M enalaprilat, an angiotensin converting enzyme inhibitor,

37 educing fetal systolic load with infusion of enalaprilat, an angiotensin converting enzyme inhibitor,

38 ol reversed the defects in responsiveness to enalaprilat and amlodipine, suggesting that inactivation

39 hase, attenuated the response to bradykinin, enalaprilat and amlodipine.

40 alone had no effect, but the combination of enalaprilat and chymostatin almost completely inhibited

41 We found that enalaprilat and other ACE inhibitors in nanomolar concen

42 terstitial administration of ACE inhibitors (enalaprilat and perindoprilat).

43 Enalaprilat and phosphoramidon were used to evaluate the

44 tiazem, and amlodipine or the ACE inhibitors enalaprilat and ramiprilat.

45 e II/angiotensin-converting enzyme inhibitor enalaprilat and the addition of kininogen or kallikrein

46 the mechanism of action of the ACE inhibitor enalaprilat and the AT1 antagonist losartan on regional

47 The ACE inhibitor enalaprilat and the peptide ligand desArg(10)-kallidin (

48 Addition of bradykinin, enalaprilat, and amlodipine decreased oxygen consumption

49 Bradykinin, enalaprilat, and amlodipine significantly suppressed cor

50 r tempol restored the ability of bradykinin, enalaprilat, and amlodipine to suppress oxygen consumpti

51 labetalol, esmolol, nicardipine, nifedipine, enalaprilat, and minoxidil.

52 After IC enalaprilat, Ang II production fell to 436+/-66.8 pg/min

53 Neither propranolol nor enalaprilat attenuated the ATL-mediated vasodilation (22

54 Enalaprilat attenuates beta-adrenergic contractility and

55 Pretreatment with enalaprilat attenuates the manifestations of myocardial

56 Enalaprilat augments both arterial and cardiopulmonary b

57 ant inhibition of BFU-E growth with 10 ng/ml enalaprilat, but controls showed no inhibition of BFU-E

58 Finally, enalaprilat, but not the prodrug enalapril, decreased in

59 In addition, unlike desArg(10)-kallidin, enalaprilat can also release NO independent of Ca(2+) in

60 ow reserve (CFR) (baseline CFR, 1.89+/-0.11; enalaprilat CFR, 2.74+/-0.33; P<0.05) in DCM.

61 rfusion was significantly enhanced in the IR-enalaprilat cohort (59 +/- 10 mL/min) compared with the

62 Resting FVR decreased during enalaprilat compared with vehicle or HOE 140, but not co

63 In the rabbit, enalaprilat completely inhibited the Ang I response.

64 nted to investigate whether these effects of enalaprilat could result into a significant clinical ben

65 Co-infusion with enalaprilat decreased +dP/dt to 26 +/- 12% and Ecs to -2

66 Enalaprilat decreased systolic blood pressure in patient

67 Enalaprilat decreased the IC50 of [Hyp3-Tyr(Me)8]BK, the

68 creased in patients with heart failure after enalaprilat despite reductions in central venous pressur

69 Enalaprilat did not alter either resting coronary tone o

70 Enalaprilat did not alter either resting coronary vascul

71 th normal left ventricular function (n = 5), enalaprilat did not inhibit contractility or reduce LVED

72 ls after PCI were significantly lower in the enalaprilat group (p < 0.001).

73 - 6% for the IR-saline, IR-captopril, and IR-enalaprilat groups, respectively (P < .05, IR-captopril

74 Intracoronary enalaprilat improves coronary microvascular function and

75 The ACE inhibitor enalaprilat improves transmural myocardial perfusion at

76 sympathetic nerve activity was unchanged by enalaprilat in control subjects.

77 eflex control of heart rate was unchanged by enalaprilat in either group.

78 Infusion with L-NMMA before enalaprilat in patients with DCM (n = 5) prevented the r

79 In a subset of 6 patients, enalaprilat increased coronary blood flow during infusio

80 Enalaprilat increased the effect of exogenous bradykinin

81 Enalaprilat increased the t-PA response to bradykinin to

82 We tested the hypothesis that enalaprilat induces preconditioning (PC)-mimetic actions

83 In contrast, reducing fetal systolic load by enalaprilat infusion slowed t-tubule development and dec

84 ter acute blockade of ANG II formation by iv enalaprilat injection in sodium-restricted animals, ANG

85 opril (IR-captopril, n = 6), or 1.5 mg/kg IV enalaprilat (IR-enalaprilat, n = 6) before 1 hour of rep

86 ril, n = 6), or 1.5 mg/kg IV enalaprilat (IR-enalaprilat, n = 6) before 1 hour of reperfusion.

87 investigated the influence of intracoronary enalaprilat on coronary microvascular function and peri-

88 his study sought to determine the effects of enalaprilat on reflex control of sympathetic nerve activ

89 We studied this effect of enalaprilat on the binding of [3H]BK to Chinese hamster

90 e also performed to determine the effects of enalaprilat on the de novo formation of RIF AngII elicit

91 tin (Ep), angiotensin II (AII), and the ACEI enalaprilat on the in vitro proliferation of erythroid p

92 In human vessels, enalaprilat or chymostatin alone had no effect, but the

93 There was no effect of enalaprilat or HOE 140 on the FBF or t-PA response to me

94 e randomized to an intracoronary infusion of enalaprilat or placebo, followed 10 min later by a PC pr

95 kininogen (10 micrograms/mL) and captopril, enalaprilat, or ramiprilat (10(-4) mol/L) reduced cardia

96 ams/mL) and three ACE inhibitors (captopril, enalaprilat, or ramiprilat; 10(-8) mol/L) increased nitr

97 ated (3+/-2%) with pacing in the presence of enalaprilat (p = 0.002).

98 .05 and was reduced to 0.042+/-0.02 after IC enalaprilat (P<0.01).

99 032 but was reduced to 0.06+/-0.01 during IC enalaprilat (P<0.01).

100 e of bioactive chemical templates, including enalaprilat, perindoprilat, endomorphin-2 and isoniazid,

101 Enalaprilat preserved a portion of the receptors in high

102 In contrast, enalaprilat-pretreated patients showed no change in ST-s

103 In addition, intracoronary enalaprilat reduced left ventricular end-diastolic press

104 Either captopril or enalaprilat restored ADP and A23187 arteriolar responses

105 Infusion of enalaprilat resulted in a significant reduction in index

106 In contrast, enalaprilat significantly increased resting net t-PA rel

107 In contrast, enalaprilat stimulates only the influx of extracellular

108 After suppression of Ang II production with enalaprilat, there was net uptake of Ang-(1-7): -289+/-1

109 Interstitial infusion of enalaprilat through the microdialysis probe (1 or 10 mM

110 Addition of enalaprilat to the perfusate (10 mM) prevented the conve

111 one to determine the effects of propranolol, enalaprilat, verapamil, and caffeine on the vasodilatory

112 In CHO-3B cells, enalaprilat was ineffective.

113 The effect of enalaprilat was studied in eight patients with PTE and e

114 old animals, the responses to bradykinin and enalaprilat were attenuated (bradykinin: 0 +/- 0% to -13

115 The effects of enalaprilat were bradykinin mediated and NO dependent an