ライフサイエンスコーパス: endothelium-dependent relaxation

1 sic coronary artery disease risk factors and endothelium-dependent relaxation.

2 stradiol plus progesterone did not influence endothelium-dependent relaxation.

3 ha release, and improved coronary arteriolar endothelium-dependent relaxation.

4 howed increased aortic stiffness and reduced endothelium-dependent relaxation.

5 oxidase, decreased O2*- levels, and improved endothelium-dependent relaxation.

6 gs had no deterioration in contraction or in endothelium-dependent relaxation.

7 dothelial cell hydrogen peroxide release, or endothelium-dependent relaxation.

8 er the onset of sepsis improves or maintains endothelium-dependent relaxation.

9 ial O2-. levels is not sufficient to improve endothelium-dependent relaxation.

10 of superoxide dismutase (SOD) would improve endothelium-dependent relaxation.

11 nd estradiol plus progesterone do not affect endothelium-dependent relaxation.

12 ed SOD, or cis-vaccenic acid did not augment endothelium-dependent relaxations.

13 ar function was measured via contraction and endothelium-dependent relaxation after stimulation with

14 d preservation of vascular smooth muscle and endothelium-dependent relaxations after prolonged hypoth

15 evels, resulting in reduced O2- and improved endothelium-dependent relaxation and basal NO release in

16 hyperpolarization, because in many arteries endothelium-dependent relaxation and hyperpolarization r

17 38 prevented NADP(H) depletion and preserved endothelium-dependent relaxation and NO generation with

18 t to diabetes mellitus-induced impairment in endothelium-dependent relaxation and reendothelializatio

19 cy due to ET-1-induced O2- leads to impaired endothelium-dependent relaxation and that gene transfer

20 during diabetes by suppressing impairment of endothelium-dependent relaxation and that protection by

21 ich restored NO bioavailability and improved endothelium-dependent relaxations and HDL endothelium-pr

22 LPS or iNOS expression has little effect on endothelium-dependent relaxation, and eNOS activity does

23 gonist SR141716A (10 microM) also attenuated endothelium-dependent relaxations but this inhibition wa

24 yme A (HMG CoA) reductase inhibitors improve endothelium-dependent relaxation by increasing ecNOS act

25 cids and GLP-1 were associated with improved endothelium-dependent relaxation compared with sham-oper

26 n human internal mammary arteries, depressed endothelium-dependent relaxations could not be attribute

27 2-CreNox2KO mice, along with preservation of endothelium-dependent relaxation during angiotensin II s

28 whether this agent attenuates the depressed endothelium-dependent relaxation during early sepsis.

29 ic tone was significantly potentiated, while endothelium-dependent relaxation (EDR) was impaired in s

30 ase-derived O2- contributes to impairment of endothelium-dependent relaxation (EDR).

31 P<.001), which was associated with impaired endothelium-dependent relaxations (EDRs) in aortic rings

32 vinblastine, their arteries maintained full endothelium-dependent relaxation, even after very high t

33 endothelium and smooth muscle contributes to endothelium-dependent relaxations evoked by both recepto

34 however, fibrinogen (0-2 microM) affected an endothelium-dependent relaxation, followed by recontract

35 significantly improved acetylcholine-induced endothelium-dependent relaxation in AMPKalpha2(-/-) mice

36 s demonstrated a significant preservation of endothelium-dependent relaxation in animals treated with

37 ion of l-sepiapterin normalized the impaired endothelium-dependent relaxation in aortas isolated from

38 Development of endothelium-dependent relaxation in canine coronary coll

39 ease in STIM1 protein expression, attenuates endothelium-dependent relaxation in diabetic coronary ar

40 of antioxidants, which are known to improve endothelium-dependent relaxation in HC, smooth muscle SE

41 osure to lucigenin resulted in inhibition of endothelium-dependent relaxation in isolated aortic ring

42 stress and SERCA oxidation and improved the endothelium-dependent relaxation in isolated mouse aorta

43 lose inspection reveals a specific effect on endothelium-dependent relaxation in mesenteric resistanc

44 Hyperglycemia attenuates endothelium-dependent relaxation in normal rabbit arteri

45 In conclusion, reduced endothelium-dependent relaxation in OHF mesenteric arter

46 We also observed impaired endothelium-dependent relaxation in resistant vessels fr

47 e control, exhibited striking improvement in endothelium-dependent relaxation in response to acetylch

48 Endothelium-dependent relaxation in response to acetylch

49 ed after 2 months exhibited markedly reduced endothelium-dependent relaxation in response to acetylch

50 Endothelium-dependent relaxation in response to shear st

51 ivity of the vasculature and to the impaired endothelium-dependent relaxation in the diseased kidney.

52 KATP channel mechanism, whereas PC preserves endothelium-dependent relaxation in the subepicardium th

53 at this time point, diabetes did not impair endothelium-dependent relaxation in vessels in wild-type

54 VHF rats (VHF vs. VC, P < 0.05) and blunted endothelium-dependent relaxation in VHF and PHF rats (VH

55 rom E also revealed a better preservation of endothelium-dependent relaxation in vitro (maximum relax

56 ed peptides (SFLLRN and SLIGRL) both induced endothelium-dependent relaxations in PGF2alpha-contracte

57 Thrombin and trypsin both elicited endothelium-dependent relaxations in prostaglandin F2alp

58 Impaired endothelium-dependent relaxations in renal arteries, car

59 mice exhibited an accelerated impairment of endothelium-dependent relaxations in response to in vitr

60 ion fully reversed the acetylcholine-induced endothelium-dependent relaxations in vitro.

61 finding that both trypsin and SLIGRL induced endothelium-dependent relaxations indicates the presence

62 Endothelium-dependent relaxation induced by acetylcholin

63 These results indicate that endothelium-dependent relaxation induced by ACh was sign

64 heterozygout mice (db/m) mice and effects on endothelium-dependent relaxation, insulin sensitivity, a

65 Functionally, acetylcholine-induced, endothelium-dependent relaxation is impaired in T1DM mes

66 pothesis that hypoxia-induced attenuation of endothelium-dependent relaxation is mediated by alterati

67 Studies have shown that endothelium-dependent relaxation (mediated by endotheliu

68 exhibit augmented contraction and diminished endothelium-dependent relaxation, most likely due to dec

69 Acetylcholine-induced endothelium-dependent relaxation of aortas after precont

70 Substance P caused an endothelium-dependent relaxation of atrial arterioles th

71 Therefore, we studied endothelium-dependent relaxation of canine collateral ar

72 After 4 months, endothelium-dependent relaxation of collateral arteries

73 Endothelium-dependent relaxation of collateral arteries

74 reduced ejection fraction, mitral E/A ratio, endothelium-dependent relaxation of coronary arteries, t

75 with preserved left ventricular function and endothelium-dependent relaxation of coronary microvessel

76 st-stimulated production of nitric oxide and endothelium-dependent relaxation of isolated blood vesse

77 The loss of endothelium-dependent relaxation of microvessels from th

78 Endothelium-dependent relaxation of porcine coronary art

79 The enhanced endothelium-dependent relaxation of rings from 17betaE(2

80 emporal profile of Ca(2+) dynamics underlies endothelium-dependent relaxation of swine coronary arter

81 re no acute changes in BP or the NO-mediated endothelium-dependent relaxation of the brachial artery

82 Since arachidonic acid causes endothelium-dependent relaxations of coronary arteries t

83 Hcy impaired endothelium-dependent relaxations of rat aortae and led

84 ived hyperpolarizing factor (EDHF)-mediated, endothelium-dependent relaxations of small mesenteric ar

85 HC and ETS significantly reduced endothelium-dependent relaxation (p = 0.01 and p < 0.000

86 Testosterone reduced endothelium-dependent relaxation (p = 0.049) and augment

87 the Ca(2+) concentration in the ER, and (3) endothelium-dependent relaxation that was attenuated in

88 l stimuli acetylcholine or bradykinin evoked endothelium-dependent relaxation that was similar in con

89 endothelium and is associated with impaired endothelium-dependent relaxation, the effects of micromo

90 nses to cyclopiazonic acid, which stimulates endothelium-dependent relaxation through a receptor-inde

91 Endothelium-dependent relaxation to acetylcholine (3x10(

92 In-utero SHS exposure reduced maximal endothelium-dependent relaxation to acetylcholine (p=0.0

93 abetes caused a 25% reduction in NO-mediated endothelium-dependent relaxation to acetylcholine for ao

94 Endothelium-dependent relaxation to acetylcholine was at

95 Endothelium-dependent relaxation to acetylcholine was bl

96 ed contractile responses to UTP and enhanced endothelium-dependent relaxation to calcium ionophore A2

97 Application of GRGDNP had no effect on endothelium-dependent relaxation to substance P (10(-12)

98 grity of the endothelium was assessed by the endothelium-dependent relaxation to substance P in a pai

99 with superoxide dismutase plus sepiapterin, endothelium-dependent relaxations to A23187, as well as

100 Endothelium-dependent relaxations to bradykinin and acet

101 on endothelium of pigs selectively augments endothelium-dependent relaxations to bradykinin by incre

102 In sepiapterin-treated arteries, endothelium-dependent relaxations to calcium ionophore A

103 ls, (2) angiotensin receptors do not mediate endothelium-dependent relaxations to the heptapeptide, a

104 (2) to amplify the ROS-induced impairment of endothelium-dependent relaxation via reduction of nitric

105 Endothelium-dependent relaxation was enhanced in male CF

106 postexperimental coronary arteries, maximal endothelium-dependent relaxation was greater in CP+GSH t

107 The contribution of gap junctions to endothelium-dependent relaxation was investigated in iso

108 Vasodilator prostanoid contribution to endothelium-dependent relaxation was reduced in lobar ar

109 ared to the wild type, acetylcholine-induced endothelium-dependent relaxation was significantly impai

110 Acetylcholine-induced endothelium-dependent relaxation was similar in all grou

111 reendothelialization of the damaged vessel, endothelium-dependent relaxation was tested in isolated

112 eotide regulatory (Gi) protein can result in endothelium-dependent relaxation, we tested the hypothes

113 Endothelium-dependent relaxations were also studied afte

114 Basal arterial NO release and endothelium-dependent relaxations were impaired in DOCA-

115 helium-independent and prostacyclin-mediated endothelium-dependent relaxations were not changed.

116 els also demonstrated significantly impaired endothelium-dependent relaxation whereas the E1/E4-AV ve

117 choline and bradykinin both led to dose- and endothelium-dependent relaxation which was unaffected by

118 gh glucose in vitro induced an impairment of endothelium-dependent relaxations, which was prevented b

119 sels from apoE(-/-) mice, uric acid improved endothelium-dependent relaxation while having no effect

120 cant time- and titer-dependent impairment in endothelium-dependent relaxation, with no effect on cont