ライフサイエンスコーパス: resistance vessel

1 ses to intraluminal pressure was examined in resistance vessels.

2 re conducted to analyze the vascular tone of resistance vessels.

3 re expressed in smooth muscle cells of small resistance vessels.

4 ectrical conduction along the endothelium of resistance vessels.

5 inc that affects myogenic reflex in systemic resistance vessels.

6 he epicardial conductance and the arteriolar resistance vessels.

7 n K+-induced vasorelaxation in human forearm resistance vessels.

8 n of vascular smooth muscle cells from renal resistance vessels.

9 muscle cells (VSMCs) of the small pulmonary resistance vessels.

10 e in regulating vascular tone, especially in resistance vessels.

11 olites of AA contribute to dilation of human resistance vessels.

12 ensin II (ANG II) receptor subtypes in renal resistance vessels.

13 f vascular ACE activity in the human forearm resistance vessels.

14 dilating systemic capacitance and pulmonary resistance vessels although only marginally dilating res

15 In rat pulmonary artery resistance vessels, an initial event in HPV is a release

16 Since changes in resistance vessel and microvascular function often prece

17 are juxtaposed to the wall of intracerebral resistance vessels and are a powerful source of reactive

18 omyocytes, skeletal myocytes, and mesenteric resistance vessels and are sufficient to confer blood pr

19 , blocked the vasodilatory action of H2O2 on resistance vessels and resulted in hypertension in vivo.

20 ments were performed on rat pulmonary artery resistance vessels and single smooth muscle cells isolat

21 rinsic hypoxic vasoconstriction of pulmonary resistance vessels, and (3) potential local and central

22 ension decorated B cells in lymphoid tissue, resistance vessels, and adventitia of large vessels.

23 othelial function both of the epicardial and resistance vessels, and leads to a reduction in myocardi

24 eased smooth muscle medial area in pulmonary resistance vessels, and significantly higher right ventr

25 ; whether ADO acts on KATP channels in these resistance vessels; and the contribution of cAMP/protein

26 Resistance vessels are assumed to respond to changes in

27 Large resistance vessels are dilated to maintain a high blood

28 on of glyceryltrinitrate-induced dilation of resistance vessels at 60 minutes of reperfusion.

29 We investigated the effect of PVAT on resistance vessel biology in male and female 16 week old

30 t (radial artery flow-mediated dilation) and resistance vessels (blood flow responses to intra-arteri

31 ectrical conduction along the endothelium of resistance vessels by governing signal dissipation throu

32 pressure-induced contractility of mesenteric resistance vessels by influencing the activity of myosin

33 of endothelium-denuded rat pulmonary artery resistance vessels caused either a sustained or transien

34 ysiological diversity is that K(Dr)-enriched resistance vessels constrict to hypoxia, whereas conduit

35 conduit and resistance artery responses and resistance vessel constriction was found with increasing

36 tensin system and directly controls vascular resistance, vessel contractility, and remodeling.

37 We hypothesized that resistance vessels develop resilience to oxidative stres

38 Forearm resistance vessel dilatation to acetylcholine was signif

39 not obligatory for exercise-induced coronary resistance vessel dilation.

40 ine loading rapidly impairs both conduit and resistance vessel endothelial function in healthy humans

41 Patients with OSA have an impairment of resistance-vessel endothelium-dependent vasodilation.

42 artery (a muscular conduit artery), forearm resistance vessels (forearm blood flow), and systemic he

43 Resistance vessels from patients with (n=12) and without

44 Epicardial and resistance vessel function in the transplanted heart has

45 Disordered resistance vessel function may account in part for reduc

46 Pulmonary arterial resistance vessel function was studied within the distri

47 ith HC-induced impairment of intramyocardial resistance vessel function.

48 RIPC increases conduit and resistance vessel function; however, the effect of RIPC

49 Resistance-vessel function was tested by use of forearm

50 nd hypertrophy or hyperplasia of conduit and resistance vessels in certain subjects.

51 ertension on contiguous coronary conduit and resistance vessels in humans.

52 ndothelium-dependent vasodilation of forearm resistance vessels in patients with insulin-dependent di

53 that Cav-1 plays a role in autoregulation of resistance vessels in the retina.

54 Thus, in human arterial resistance vessels in vitro, BRL 49653 does not possess

55 endothelium-dependent vasodilators, both in resistance vessels in vivo and in the carotid artery ex

56 ide to relax smooth muscle cells surrounding resistance vessels in vivo is well documented.

57 NO bioavailability that dynamically dilated resistance vessels in vivo under basal conditions withou

58 asodilation, preferentially of preglomerular resistance vessels, increasing both renal blood flow and

59 Whereas smooth muscle contraction of resistance vessels is enhanced by noradrenaline release

60 the myogenic tone of third-order mesenteric resistance vessels is increased, the vascular smooth mus

61 uced coronary vasodilation of epicardial and resistance vessels is mediated in part by endothelium-de

62 Smoking-induced endothelial dysfunction of resistance vessels is rapidly reversed with oral allopur

63 Endothelial dysfunction in conduit and resistance vessels may underlie the reported association

64 Vascular tone in the resistance vessel mechanics model is governed by input s

65 etate for NO activity in isolated mesenteric resistance vessels (MRVs).

66 cular reactivity was measured in the forearm resistance vessels of 21 patients with non-insulin-depen

67 he predominant ANG II receptor type in renal resistance vessels of 7-wk-old rats.

68 local NEP causes vasoconstriction in forearm resistance vessels of both healthy volunteers and patien

69 verexpressed in smooth muscle cells of renal resistance vessels of hypertensive salt-sensitive rats a

70 ver 1 hour) on vasomotor function in forearm resistance vessels of patients with coronary artery dise

71 s ET-1 on ET(A) receptors is enhanced in the resistance vessels of patients with diabetes, whereas th

72 ioxidant, on vasodilator function in forearm resistance vessels of patients with hypercholesterolemia

73 helium-dependent vasodilation in the forearm resistance vessels of patients with hypercholesterolemia

74 helium-dependent vasodilation in the forearm resistance vessels of patients with insulin-dependent di

75 lude that endothelial dysfunction in forearm resistance vessels of patients with non-insulin-dependen

76 ndothelium-dependent vasodilation in forearm resistance vessels of patients with non-insulin-dependen

77 nitric oxide and endothelin-1 in peripheral resistance vessels of patients with syndrome X.

78 vely blocks AT1A and AT1B receptors in renal resistance vessels of rodents, with similar efficacies i

79 caused reproducible vasodilation in forearm resistance vessels (p < 0.0001).

80 endothelial dysfunction in both conduit and resistance vessels (P=0.03).

81 Changes in coronary blood flow (a measure of resistance vessel reactivity) and coronary artery diamet

82 of the epicardial coronary arteries and the resistance vessels relative to metabolic demand.

83 lium-independent dilators NTG and verapamil (resistance vessel response).

84 occlusion plethysmography was used to assess resistance vessel responses (16 hours before and 8 hours

85 Eight hours after vaccination, resistance vessel responses to BK (P:=0.0099) and ACh (P

86 Thirty-two hours after vaccination, resistance vessel responses to BK and ACh had returned t

87 Resistance vessel responses to verapamil and NTG were un

88 In forearm resistance vessels, SFLLRN increased forearm blood flow

89 ce vessels although only marginally dilating resistance vessels, sodium nitrite (NaNO2) infusion woul

90 and relative wave reflection (correlates of resistance vessel structure and function) were not assoc

91 trophic hormonal changes that can influence resistance vessel structure and, consequently, blood pre

92 Arterial baroreflexes may regulate resistance vessels supplying glucose to skeletal muscle

93 g pregnancy transforms them from high to low resistance vessels that lack vasoconstrictive properties

94 % to 3.5+/-0.9%) and the dilator response of resistance vessels to acetylcholine at 15, 30, and 60 mi

95 a requisite role in constriction of coronary resistance vessels to alpha1-adrenergic stimuli, which m

96 ased flow velocity sufficiently in the major resistance vessels to cause a flow-mediated release of n

97 an impaired vasodilator response of coronary resistance vessels to increased sympathetic stimulation,

98 ts, as a key molecular mechanism sensitizing resistance vessels to pressure-induced vasoconstriction

99 ys fed normal diet (P = 0.008), Responses of resistance vessels to the endothelium-dependent vasodila

100 degree of intrinsic tone in conductance and resistance vessels, to define the calcium dependency of

101 role (if any) of K(IR) in controlling human resistance vessel tone is unknown, and we investigated t

102 ffects of local inhibition of NEP on forearm resistance vessel tone.

103 generation is important in the regulation of resistance vessel tone.

104 Endothelial function of forearm resistance vessels was assessed by use of forearm vasodi

105 h sildenafil caused vasodilation of coronary resistance vessels with an increase of blood flow into a