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1 re expressed in smooth muscle cells of small resistance vessels.
2 ectrical conduction along the endothelium of resistance vessels.
3 inc that affects myogenic reflex in systemic resistance vessels.
4 he epicardial conductance and the arteriolar resistance vessels.
5 n K+-induced vasorelaxation in human forearm resistance vessels.
6 n of vascular smooth muscle cells from renal resistance vessels.
7  muscle cells (VSMCs) of the small pulmonary resistance vessels.
8 e in regulating vascular tone, especially in resistance vessels.
9 olites of AA contribute to dilation of human resistance vessels.
10 ensin II (ANG II) receptor subtypes in renal resistance vessels.
11 f vascular ACE activity in the human forearm resistance vessels.
12  dilating systemic capacitance and pulmonary resistance vessels although only marginally dilating res
13                      In rat pulmonary artery resistance vessels, an initial event in HPV is a release
14  are juxtaposed to the wall of intracerebral resistance vessels and are a powerful source of reactive
15 omyocytes, skeletal myocytes, and mesenteric resistance vessels and are sufficient to confer blood pr
16 , blocked the vasodilatory action of H2O2 on resistance vessels and resulted in hypertension in vivo.
17 ments were performed on rat pulmonary artery resistance vessels and single smooth muscle cells isolat
18 rinsic hypoxic vasoconstriction of pulmonary resistance vessels, and (3) potential local and central
19 ension decorated B cells in lymphoid tissue, resistance vessels, and adventitia of large vessels.
20 othelial function both of the epicardial and resistance vessels, and leads to a reduction in myocardi
21 eased smooth muscle medial area in pulmonary resistance vessels, and significantly higher right ventr
22 ; whether ADO acts on KATP channels in these resistance vessels; and the contribution of cAMP/protein
23                                              Resistance vessels are assumed to respond to changes in
24                                        Large resistance vessels are dilated to maintain a high blood
25 on of glyceryltrinitrate-induced dilation of resistance vessels at 60 minutes of reperfusion.
26 t (radial artery flow-mediated dilation) and resistance vessels (blood flow responses to intra-arteri
27 ectrical conduction along the endothelium of resistance vessels by governing signal dissipation throu
28  of endothelium-denuded rat pulmonary artery resistance vessels caused either a sustained or transien
29 ysiological diversity is that K(Dr)-enriched resistance vessels constrict to hypoxia, whereas conduit
30  conduit and resistance artery responses and resistance vessel constriction was found with increasing
31 tensin system and directly controls vascular resistance, vessel contractility, and remodeling.
32                                      Forearm resistance vessel dilatation to acetylcholine was signif
33 not obligatory for exercise-induced coronary resistance vessel dilation.
34 ine loading rapidly impairs both conduit and resistance vessel endothelial function in healthy humans
35      Patients with OSA have an impairment of resistance-vessel endothelium-dependent vasodilation.
36  artery (a muscular conduit artery), forearm resistance vessels (forearm blood flow), and systemic he
37                                              Resistance vessels from patients with (n=12) and without
38                               Epicardial and resistance vessel function in the transplanted heart has
39                                   Disordered resistance vessel function may account in part for reduc
40                           Pulmonary arterial resistance vessel function was studied within the distri
41 ith HC-induced impairment of intramyocardial resistance vessel function.
42                                              Resistance-vessel function was tested by use of forearm
43 nd hypertrophy or hyperplasia of conduit and resistance vessels in certain subjects.
44 ertension on contiguous coronary conduit and resistance vessels in humans.
45 ndothelium-dependent vasodilation of forearm resistance vessels in patients with insulin-dependent di
46 that Cav-1 plays a role in autoregulation of resistance vessels in the retina.
47                      Thus, in human arterial resistance vessels in vitro, BRL 49653 does not possess
48  endothelium-dependent vasodilators, both in resistance vessels in vivo and in the carotid artery ex
49 ide to relax smooth muscle cells surrounding resistance vessels in vivo is well documented.
50  NO bioavailability that dynamically dilated resistance vessels in vivo under basal conditions withou
51 asodilation, preferentially of preglomerular resistance vessels, increasing both renal blood flow and
52         Whereas smooth muscle contraction of resistance vessels is enhanced by noradrenaline release
53  the myogenic tone of third-order mesenteric resistance vessels is increased, the vascular smooth mus
54 uced coronary vasodilation of epicardial and resistance vessels is mediated in part by endothelium-de
55   Smoking-induced endothelial dysfunction of resistance vessels is rapidly reversed with oral allopur
56       Endothelial dysfunction in conduit and resistance vessels may underlie the reported association
57 etate for NO activity in isolated mesenteric resistance vessels (MRVs).
58 cular reactivity was measured in the forearm resistance vessels of 21 patients with non-insulin-depen
59 he predominant ANG II receptor type in renal resistance vessels of 7-wk-old rats.
60 local NEP causes vasoconstriction in forearm resistance vessels of both healthy volunteers and patien
61 ver 1 hour) on vasomotor function in forearm resistance vessels of patients with coronary artery dise
62 s ET-1 on ET(A) receptors is enhanced in the resistance vessels of patients with diabetes, whereas th
63 ioxidant, on vasodilator function in forearm resistance vessels of patients with hypercholesterolemia
64 helium-dependent vasodilation in the forearm resistance vessels of patients with hypercholesterolemia
65 helium-dependent vasodilation in the forearm resistance vessels of patients with insulin-dependent di
66 ndothelium-dependent vasodilation in forearm resistance vessels of patients with non-insulin-dependen
67 lude that endothelial dysfunction in forearm resistance vessels of patients with non-insulin-dependen
68  nitric oxide and endothelin-1 in peripheral resistance vessels of patients with syndrome X.
69 vely blocks AT1A and AT1B receptors in renal resistance vessels of rodents, with similar efficacies i
70  caused reproducible vasodilation in forearm resistance vessels (p < 0.0001).
71  endothelial dysfunction in both conduit and resistance vessels (P=0.03).
72 Changes in coronary blood flow (a measure of resistance vessel reactivity) and coronary artery diamet
73  of the epicardial coronary arteries and the resistance vessels relative to metabolic demand.
74 lium-independent dilators NTG and verapamil (resistance vessel response).
75 occlusion plethysmography was used to assess resistance vessel responses (16 hours before and 8 hours
76               Eight hours after vaccination, resistance vessel responses to BK (P:=0.0099) and ACh (P
77          Thirty-two hours after vaccination, resistance vessel responses to BK and ACh had returned t
78                                              Resistance vessel responses to verapamil and NTG were un
79                                   In forearm resistance vessels, SFLLRN increased forearm blood flow
80 ce vessels although only marginally dilating resistance vessels, sodium nitrite (NaNO2) infusion woul
81  and relative wave reflection (correlates of resistance vessel structure and function) were not assoc
82  trophic hormonal changes that can influence resistance vessel structure and, consequently, blood pre
83           Arterial baroreflexes may regulate resistance vessels supplying glucose to skeletal muscle
84 g pregnancy transforms them from high to low resistance vessels that lack vasoconstrictive properties
85 % to 3.5+/-0.9%) and the dilator response of resistance vessels to acetylcholine at 15, 30, and 60 mi
86 a requisite role in constriction of coronary resistance vessels to alpha1-adrenergic stimuli, which m
87 ased flow velocity sufficiently in the major resistance vessels to cause a flow-mediated release of n
88 an impaired vasodilator response of coronary resistance vessels to increased sympathetic stimulation,
89 ts, as a key molecular mechanism sensitizing resistance vessels to pressure-induced vasoconstriction
90 ys fed normal diet (P = 0.008), Responses of resistance vessels to the endothelium-dependent vasodila
91  degree of intrinsic tone in conductance and resistance vessels, to define the calcium dependency of
92  role (if any) of K(IR) in controlling human resistance vessel tone is unknown, and we investigated t
93 ffects of local inhibition of NEP on forearm resistance vessel tone.
94 generation is important in the regulation of resistance vessel tone.
95              Endothelial function of forearm resistance vessels was assessed by use of forearm vasodi
96 h sildenafil caused vasodilation of coronary resistance vessels with an increase of blood flow into a

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