ライフサイエンスコーパス: EDHF

1 EDHF candidates include cytochrome P-450 metabolites of

2 EDHF is the major contributor to endothelium-dependent v

3 EDHF signals radially from the endothelium to cause dila

4 EDHF was found to account for approximately 80% of acety

5 EDHF-mediated vasorelaxation, however, was sensitive to

6 t an inhibitory interaction exists between 2 EDHFs in the human coronary microcirculation.

7 are consistent with the idea that H2O2 is an EDHF that contributes to FID in HCA from patients with h

8 nhibitors improved endothelium-dependent and EDHF-mediated relaxations and decreased O(2)(-) producti

9 underlying the relaxation evoked by K(+) and EDHF were elucidated.

10 The basal and stimulated releases of NO and EDHF-mediated hyperpolarization in the IMA are significa

11 ata support the hypothesis that the EETs are EDHFs.

12 These findings support a role of EETs as EDHFs.

13 atrienoic acids (EETs) appear to function as EDHFs.

14 Because EDHF activity is a principal determinant of vasorelaxati

15 channel (K(Ca)) inhibitor completely blocked EDHF-mediated relaxation.

16 ever, they appeared to be mediated mainly by EDHF rather than by EDNO as in the low salt animals.

17 Hyperpolarization of smooth muscle by EDHF is also abolished by this toxin combination, but th

18 Under control conditions EDHF-type relaxations evoked by acetylcholine (ACh) in r

19 ute to endothelial dysfunction and defective EDHF-dependent relaxation.

20 residues 130 to 140) each markedly depressed EDHF-mediated dilation.

21 othesis that elevation of cAMP would enhance EDHF-mediated dilations in female rat MCA.

22 xation, whereas RGS2 sufficiency facilitates EDHF-evoked relaxation by squelching endothelial G(i/o)

23 endothelium derived hyperpolarising factor (EDHF) with apamin and charybdotoxin.

24 endothelium-derived hyperpolarising factor (EDHF).

25 dent transferrable hyperpolarization factor (EDHF) in response to shear stress.

26 endothelium-derived hyperpolarizing factor (EDHF) are significantly attenuated in the middle cerebra

27 endothelium-derived hyperpolarizing factor (EDHF) contributes to microvascular dilation more than ni

28 ndothelium-dependent hyperpolarizing factor (EDHF) pathway.

29 endothelium-derived hyperpolarizing factor (EDHF) which is neither prostacyclin nor nitric oxide.

30 endothelium-derived hyperpolarizing factor (EDHF), and both mechanisms are impaired by diabetes.

31 endothelium-derived hyperpolarizing factor (EDHF), is more prevalent in resistance than in conduit b

32 endothelium-derived hyperpolarizing factor (EDHF), possibly a lipoxygenase-derived eicosanoid, and a

33 endothelium-derived hyperpolarizing factor (EDHF), that mediate the vascular effects of vasoactive h

34 endothelium-derived hyperpolarizing factor (EDHF)-dependent relaxation.

35 endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization for IMA and RA.

36 endothelium-derived hyperpolarizing factor (EDHF)-mediated, endothelium-dependent relaxations of sma

37 endothelium-derived hyperpolarizing factor (EDHF).

38 endothelium-derived hyperpolarizing factor (EDHF).

39 endothelium-derived hyperpolarizing factor (EDHF).

40 ndothelial-dependent hyperpolarizing factor (EDHF).

41 endothelium-derived hyperpolarizing factor (EDHF).

42 endothelium-derived hyperpolarizing factor (EDHF).

43 endothelium-derived hyperpolarizing factors (EDHFs) in animal vascular tissues.

44 endothelium-derived hyperpolarizing factors (EDHFs) in the human coronary microcirculation.

45 dothelial-dependent hyperpolarizing factors (EDHFs) which upregulate blood flow when tissue perfusion

46 endothelium-derived hyperpolarizing factors (EDHFs).

47 endothelium-derived hyperpolarizing factors (EDHFs).

48 Further, EDHF-mediated relaxation was inhibited by ONOO(-) and pr

49 However, EDHF played a minor role in acetylcholine-induced relaxa

50 Impaired EDHF-mediated vasodilatation was rescued by blocking G(i

51 ndothelial dysfunction resulting in impaired EDHF-dependent vasodilatation.

52 O-dependent relaxation but markedly impaired EDHF-dependent relaxation.

53 This mechanism may contribute to impaired EDHF-mediated dilation in conditions such as ischemia/re

54 n OHF mesenteric arteries is due to impaired EDHF-mediated relaxation.

55 Our results suggest that HHcy impairs EDHF relaxation in SMAs by inhibiting SK/IK activities v

56 ctly demonstrate a critical role for Cx40 in EDHF-mediated dilation of rat mesenteric arteries.

57 obe the role of endothelial gap junctions in EDHF-mediated dilation, we developed a method, which was

58 BK-induced EDHF-mediated hyperpolarization in the IMA was significa

59 ables endothelial G(i/o) activity to inhibit EDHF-dependent relaxation, whereas RGS2 sufficiency faci

60 ate-conductance K(Ca) (IK) failed to inhibit EDHF-mediated relaxation in HHcy mice.

61 We now show that H(2)S is a major EDHF because in blood vessels of CSE-deleted mice, hyper

62 H(2)S is a major EDHF that causes vascular endothelial and smooth muscle

63 hanisms underlying the vasodilator action of EDHF to elucidate its identity.

64 2) has been shown to be a major component of EDHF in several vascular beds in multiple species, inclu

65 The contribution of EDHF to the vasodilation induced by acetylcholine was as

66 The mediator responsible for the effect of EDHF is unknown.

67 t of extracellular K+ mimic these effects of EDHF in a ouabain- and Ba2+-sensitive, but endothelium-i

68 acid and not K(+) is the likely identity of EDHF in human subcutaneous resistance arteries.

69 The identity of EDHF remains unknown.

70 We studied the relative importance of EDHF, nitric oxide (NO), and prostacyclin (PGI(2)) as va

71 ilation, possibly by means of the release of EDHF.

72 membrane potential) was used to study NO or EDHF in response to acetylcholine (ACh) and bradykinin (

73 determine if H(2)S is a major physiological EDHF.

74 ed via cytochrome P450, were the predominant EDHF active in the response.

75 Our results demonstrate that reduced EDHF dilations in female rat MCA cannot be solely attrib

76 rome P450, we wondered if the EETs represent EDHFs.

77 These data suggest EDHFs are responsible for a large portion of initial pea

78 is important since it has been proposed that EDHF serves as a compensatory mechanism to maintain dila

79 These data show that EDHF is K+ that effluxes through charybdotoxin- and apam

80 Here we show that EDHF-induced hyperpolarization of smooth muscle and rela

81 lowing: (1) EET-induced relaxations, (2) the EDHF component of methacholine-induced, bradykinin-induc

82 will target other potential sites along the EDHF pathway in order to identify why EDHF dilations are

83 d the hypothesis that H(2)O(2) serves as the EDHF in HCAs to shear stress.

84 es and BKCa channels play major roles in the EDHF component of reactive hyperaemia and appear to work

85 he importance of PKGI-alpha oxidation in the EDHF mechanism and blood pressure control in vivo, we ge

86 e gap junctions appear to be involved in the EDHF pathway and cAMP has been shown to enhance gap junc

87 each) for 2 hours also failed to modify the EDHF response.

88 suggest EETs contribute to about half of the EDHF response.

89 gesting that the contribution of cAMP to the EDHF phenomenon is permissive.

90 endothelial hyperpolarization underpins the EDHF phenomenon, with cAMP governing subsequent electrot

91 ear maximal local dilatation attributable to EDHF.

92 This component of relaxation, attributed to EDHF, was significantly reduced in OHF mesenteric arteri

93 ing approximately 40% could be attributed to EDHF-mediated activation of KCa channels, and whether th

94 of H(2)O(2), which acts as the transferrable EDHF activating BK(Ca) channels on the smooth muscle cel

95 and H2O2 in human coronary arterioles, where EDHF-mediated vasodilatory mechanisms are prominent.

96 as not apparent in femoral arteries in which EDHF has a less prominent role.

97 ng the EDHF pathway in order to identify why EDHF dilations are reduced in the female compared to the

98 peptide (CNP) has properties consistent with EDHF-like activity.