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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
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
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
34 ine loading rapidly impairs both conduit and resistance vessel endothelial function in healthy humans
36 artery (a muscular conduit artery), forearm resistance vessels (forearm blood flow), and systemic he
45 ndothelium-dependent vasodilation of forearm resistance vessels in patients with insulin-dependent di
48 endothelium-dependent vasodilators, both in resistance vessels in vivo and in the carotid artery ex
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
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
58 cular reactivity was measured in the forearm resistance vessels of 21 patients with non-insulin-depen
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
69 vely blocks AT1A and AT1B receptors in renal resistance vessels of rodents, with similar efficacies i
72 Changes in coronary blood flow (a measure of resistance vessel reactivity) and coronary artery diamet
75 occlusion plethysmography was used to assess resistance vessel responses (16 hours before and 8 hours
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
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
96 h sildenafil caused vasodilation of coronary resistance vessels with an increase of blood flow into a
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