ライフサイエンスコーパス: vasorelaxation

1 ucose utilization, and endothelium-dependent vasorelaxation.

2 for low-dose (1-10 nM) nitroglycerin-induced vasorelaxation.

3 ex vivo from WKY rats caused dose-dependent vasorelaxation.

4 K) channels, which are major determinants in vasorelaxation.

5 and play a key role in endothelium-dependent vasorelaxation.

6 ochondria, leading to production of cGMP and vasorelaxation.

7 t role for phosphorylated HSP20 in mediating vasorelaxation.

8 ion, thermosensation, mechanoregulation, and vasorelaxation.

9 to S1P and the potentiation of S1P-mediated vasorelaxation.

10 ess the mechanism by which propionate caused vasorelaxation.

11 = 40.9 +/- 5.8 %) opposed anandamide-induced vasorelaxation.

12 the type I cGMP-dependent protein kinase and vasorelaxation.

13 o eNOS activation and nitric oxide dependent vasorelaxation.

14 of RGS2 by PKG appears to contribute to this vasorelaxation.

15 as barium and ouabain reversed K(+)-mediated vasorelaxation.

16 Ca(2+) channel downregulation in NO-induced vasorelaxation.

17 ithout effects on contraction or NO-mediated vasorelaxation.

18 approximately 80% of acetylcholine-mediated vasorelaxation.

19 vity was associated with reduced NO-mediated vasorelaxation.

20 ase and the associated endothelium-dependent vasorelaxation.

21 n of HSP20 on Ser16 modulates cAMP-dependent vasorelaxation.

22 O-mediated and non-NO-mediated components of vasorelaxation.

23 P binding, namely kinase activation and thus vasorelaxation.

24 on of cytoplasmic calcium concentrations and vasorelaxation.

25 f vasoconstriction and endothelium-dependent vasorelaxation.

26 7,8-DHHD also produced vasorelaxation.

27 e production of O2.- and impair NO-dependent vasorelaxation.

28 Haw bark neither activated KCNQ5 nor induced vasorelaxation.

29 tor-induced SK current activation in ECs and vasorelaxation.

30 endothelial cells for acetylcholine-mediated vasorelaxation.

31 ced Cav1, and impaired endothelium-dependent vasorelaxation.

32 triggering cellular activity known to induce vasorelaxation.

33 l injury, and improved endothelial-dependent vasorelaxation.

34 ive stress, induce angiogenesis, and promote vasorelaxation.

35 peutic strategies by targeting cell-mediated vasorelaxation.

36 ts knock-down inhibits endothelium-dependent vasorelaxation.

37 acetylcholine-induced, nitric oxide-mediated vasorelaxation.

38 omboxane mimetic, resulted in dose-dependent vasorelaxation.

39 pressure, and impaired endothelium-dependent vasorelaxation.

40 tial for PKG activation and angiogenesis and vasorelaxation.

41 nduced vasoconstriction or carbachol-induced vasorelaxation.

42 bit glibenclamide-insensitive, H(2)S-induced vasorelaxation.

43 ramide but failed to normalize the defect in vasorelaxation.

44 emonstrate three mechanisms for zinc-induced vasorelaxation: (1) activation of transient receptor pot

45 m-dependent hyperpolarization (EDH)-mediated vasorelaxation; 2) increases glycocalyx thickness and ma

46 exchanges NO groups with ambient thiols for vasorelaxation; 2) some NO groups released from Cys(beta

47 treated mice exhibited a slight reduction in vasorelaxation ability, as well as detectable abnormalit

48 ethyl-bovine serum albumin exhibited similar vasorelaxation activity as that observed with nitrosated

49 This remaining vasorelaxation activity, termed endothelium-derived hype

50 fDNA/NETs levels and compromised endothelial vasorelaxation after CPB.

51 ted inhibition of MLC phosphatase, promoting vasorelaxation, although the molecular mechanisms that m

52 sodium nitroprusside-induced (NO-dependent) vasorelaxation and a 42% decrease in sGC expression afte

53 e in HVPG by improving flow-mediated hepatic vasorelaxation and ameliorated systemic hypotension.

54 ) mice showed impaired endothelium-dependent vasorelaxation and angiogenesis, and fibrosis occurred s

55 aortas displayed increased vasoconstriction, vasorelaxation and blood pressure were unchanged.

56 on of NO, a molecule that directly regulates vasorelaxation and blood supply.

57 release modulates endothelial cell-dependent vasorelaxation and cytokine gene expression.

58 arterial stiffness and endothelium-dependent vasorelaxation and decrease in type I IFN gene signature

59 ignificantly decreased endothelium-dependent vasorelaxation and eNOS mRNA levels, whereas it increase

60 etreatment markedly potentiated S1P-mediated vasorelaxation and eNOS Ser-1179 phosphorylation.

61 te exposure to IFNalpha impaired endothelial vasorelaxation and EPC function in lupus-prone and non-l

62 pable of releasing CO failed to promote both vasorelaxation and hypotension, thus directly implicatin

63 carboxylate were prepared and evaluated for vasorelaxation and inhibition of soluble epoxide hydrola

64 is a newly discovered factor that stimulates vasorelaxation and inhibits cell proliferation.

65 (BK-beta1), is a key determinant of coronary vasorelaxation and its function is impaired in diabetic

66 Nitrosated Gly-Trp exhibited dose-dependent vasorelaxation and platelet inhibiting activity with app

67 ndothelial cells, and induced dose-dependent vasorelaxation and reduced high-glucose or lipid-induced

68 microenvironment, can directly activate PAR2 vasorelaxation and signaling, stimulating calcium and mi

69 aMKII initiating cellular activity linked to vasorelaxation and suggests novel roles for this Ca(2+)

70 exhibit impaired nitric oxide/cGMP-dependent vasorelaxation and systemic hypertension.

71 te a Ca(2+)-independent component of hypoxic vasorelaxation and to investigate its mechanism, we util

72 R-204 rescues impaired endothelium-dependent vasorelaxation and vascular Sirt1, and decreases vascula

73 hibited both beta-blocker-induced glomerular vasorelaxations and beta-blocker-stimulated NO release f

74 Endothelium-dependent vasorelaxations and direct measurements of vascular supe

75 Furthermore, reduced endothelial vasorelaxations and increased vascular NAD(P)H oxidase a

76 S production, restored endothelium-dependent vasorelaxation, and attenuated apoptosis by limiting cyt

77 enitor cells, improved endothelium-dependent vasorelaxation, and markedly delayed time to arterial th

78 thase (eNOS), impaired endothelium-dependent vasorelaxation, and mild hypertension compared with cont

79 sociated impairment of endothelium-dependent vasorelaxation, and preserves endothelial Sirt1.

80 ative stress, improved acetylcholine-induced vasorelaxation, and reduced proteinuria in db/db recipie

81 ial nitric oxide-synthase activity, promoted vasorelaxation, and reduced vascular endothelial activat

82 es including antiinflammatory, antiplatelet, vasorelaxation, and-as a novel potent ligand of PPARgamm

83 ers from ascitic rats had significantly less vasorelaxation as compared with livers from nonascitic r

84 indicate that AT2 works in the direction of vasorelaxation as opposed to vasoconstriction by AT1.

85 ide synthase (NOS)- to neuronal NOS-mediated vasorelaxation, as well as alterations in oxidative stre

86 CB(1) or CB(2) receptors and does not cause vasorelaxation at concentrations up to 30 microM, but it

87 Consistent with waning RPTPgamma-dependent vasorelaxation at low [HCO(3)(-)], RPTPgamma limits incr

88 tnl1(-/-) mice exhibited strikingly enhanced vasorelaxation before exercise, similar in extent to tha

89 termined in transfer experiments in a murine vasorelaxation bioassay system.

90 oTEMPO), reduced blood pressure and improved vasorelaxation both in Sirt3(-/-) and wild-type mice.

91 d aortic NADPH oxidase activity and impaired vasorelaxation, both of which were prevented either by c

92 PKG) mediates classic nitric oxide-dependent vasorelaxation, but the 1alpha isoform is also independe

93 Vasorelaxation by abn-cbd is endothelium-dependent, pert

94 and smooth muscle cell hyperpolarization and vasorelaxation by activating the ATP-sensitive, intermed

95 Improvement of endothelium-dependent vasorelaxation by antibiotics is lost in mice lacking en

96 K(ATP) channel-mediated vasorelaxation by cromakalim was significantly impaired

97 Vasorelaxation by estrogens in female and male rat aorta

98 However, the exact mechanism of vasorelaxation by estrogens remains to be elucidated.

99 and-activated nuclear receptor that promotes vasorelaxation by increasing nitric oxide and downregula

100 iates hypoxic vasodilation by RBCs, and that vasorelaxation by RBCs dominates NO-based vasoconstricti

101 ults unambiguously show that hypoxia-induced vasorelaxation can occur in permeabilized arteries where

102 irrhotic liver, INT-747 improved endothelial vasorelaxation capacity, but not hyperresponsiveness.

103 ) stimulates cGMP synthesis, which regulates vasorelaxation, cell proliferation, and bone growth.

104 iferation, and (ii) promote angiogenesis and vasorelaxation, consequently providing the tumor with bl

105 Overall, substance P-induced vasorelaxation corresponded poorly with whole-field endo

106 e-induced impairment of endothelial-mediated vasorelaxation could also be reversed using gp91ds-tat.

107 -induced impairment of endothelium-dependent vasorelaxation, decrease in bioavailable nitric oxide, a

108 Mechanistically, the vasorelaxation defect was associated with decreased endo

109 ic response, and attenuated H(2)S-stimulated vasorelaxation, demonstrating the requirement of NO in v

110 uced cyclic guanylyl monophosphate-dependent vasorelaxation during hypoxia (35+/-4% at 1% O2, 4.7+/-1

111 clic guanosine monophosphate (cGMP) mediated vasorelaxation effector mechanisms in vascular smooth mu

112 The vasorelaxation elicited by acetylcholine (ACh) in phenyl

113 caused impairment of acetylcholine-dependent vasorelaxation ex vivo, which was rescued by NPR-C pharm

114 EDHF-mediated vasorelaxation, however, was sensitive to the phospholip

115 at cysteine 42 to enhance oxidant-stimulated vasorelaxation; however, the impact of PKG1alpha oxidati

116 ly refractory to cyclic nucleotide-dependent vasorelaxation, human umbilical artery smooth muscle, di

117 hear stress on endothelial cells and induced vasorelaxation in a PIEZO1-dependent manner.

118 that ceramide impairs endothelium-dependent vasorelaxation in a tissue-autonomous manner.

119 hybrid formation, restored insulin-mediated vasorelaxation in aorta, and insulin stimulated NO relea

120 We determined PRA and SIM effects on vasorelaxation in aortic rings and NO production by cult

121 associated with cyclic nucleotide-dependent vasorelaxation in bovine trachealis and carotid artery s

122 ocardial perfusion and endothelium-dependent vasorelaxation in chronically ischemic myocardium.

123 There was significantly less vasorelaxation in cirrhotic livers as compared with norm

124 racellular Ca2+ in 17 beta-estradiol-induced vasorelaxation in depolarized aortic rings, isolated fro

125 ular H(4)B content and endothelium-dependent vasorelaxation in diabetes.

126 nitric oxide (NO)-dependent and -independent vasorelaxation in healthy blacks and whites to investiga

127 in controlling basal tone and in K+-induced vasorelaxation in human forearm resistance vessels.

128 e major contributor to endothelium-dependent vasorelaxation in human subcutaneous resistance arteries

129 alcitonin gene-related peptide which elicits vasorelaxation in isolated blood vessels in vitro.

130 soconstriction or inhibition of ACh-mediated vasorelaxation in isolated human coronary arteries.

131 n vivo model of acute pulmonary embolism and vasorelaxation in isolated pulmonary arteries.

132 study sought to assess endothelium-dependent vasorelaxation in long-term users of cocaine.

133 Ialpha correlated with enhanced HNO-mediated vasorelaxation in mesenteric arteries in vitro and arter

134 ic oxide, and improves endothelium-dependent vasorelaxation in mouse aortas.

135 NO production and is required for E2-induced vasorelaxation in murine aortas.

136 BNP resulted in potent vasorelaxation in normal isolated aortic rings, which we

137 EDHF activity is a principal determinant of vasorelaxation in numerous vascular beds, drugs influenc

138 d pressure and improve endothelium-dependent vasorelaxation in patients with atherosclerosis or risk

139 entration and improves endothelium-dependent vasorelaxation in patients with coronary artery disease.

140 rectly activated by cAMP (Epac) in mediating vasorelaxation in rat mesenteric arteries.

141 Vasorelaxation in response to acetylcholine was inhibite

142 ession, increased vascular BH4, and improved vasorelaxation in response to acetylcholine, which was i

143 d vasodilator pathways; however, substantial vasorelaxation in response to agents such as acetylcholi

144 Endothelium-dependent vasorelaxation in response to bradykinin was reduced sig

145 ficantly also impaired endothelium-dependent vasorelaxation in response to bradykinin.

146 endothelium-dependent, nitric oxide-mediated vasorelaxation in response to muscarinic or proteinase-a

147 This mechanism underlies cGMP-independent vasorelaxation in response to oxidants in the cardiovasc

148 lized MAP and improved endothelium-dependent vasorelaxation in sGCalpha1-deficient mice.

149 ve factor Xa induced hypotension in rats and vasorelaxation in the isolated rat mesentery, which was

150 ncentrations (10 and 30 mumol/L) that caused vasorelaxation in the same tissue, suggesting that inhib

151 e, a high-affinity PPARgamma agonist-induced vasorelaxation in UtA preconstricted with phenylephrine,

152 ished ALDH2 inhibitors attenuate GTN-induced vasorelaxation in vitro and in vivo.

153 cular smooth muscle cells leads to prolonged vasorelaxation in vivo and contributes to the profound v

154 we investigated BNP and acetylcholine (ACh) vasorelaxations in aortic rings from normal and atherosc

155 as high plasma BH4 was associated with lower vasorelaxations in response to acetylcholine (P<0.05).

156 sis and attenuates the acetylcholine-induced vasorelaxation, indicating a partial requirement of H(2)

157 Endothelium-dependent vasorelaxation induced by a calcium ionophore (A23187) w

158 hermore, BFM improved nitric oxide-dependent vasorelaxation induced by acetylcholine in aortic rings

159 a nitric oxide synthase inhibitor, affected vasorelaxation induced by kallistatin.

160 tly contributes to the endothelium-dependent vasorelaxation induced by the KATP channel opener pinaci

161 which IL-10 preserves endothelium-dependent vasorelaxation involves O(2-), perhaps by reducing produ

162 Cyclic nucleotide-dependent vasorelaxation is associated with increases in the phosp

163 e potential mechanism of septic RBC-mediated vasorelaxation is discussed and may involve the intermed

164 Direct measurement of NO confirmed that vasorelaxation is due to NO release and showed that PRA

165 in response to norepinephrine is reduced and vasorelaxation is enhanced in response to beta-adrenergi

166 We conclude that endothelium-dependent vasorelaxation is impaired in long-term users of cocaine

167 RBC-mediated vasorelaxation is inhibited by prior depletion of S-nitr

168 The vasorelaxation is wavelength-specific, with a maximal re

169 signalled by impaired endothelium-dependent vasorelaxation, is an early marker of atherosclerosis.

170 tor signaling improved endothelium-dependent vasorelaxation, lipoprotein parameters, EPC numbers and

171 x- and estrous cycle stage-dependence of the vasorelaxation matches sex- and estrous cycle stage-depe

172 ity, indicating that Col4a1 mutations affect vasorelaxation mediated by endothelium-derived nitric ox

173 by phosphomimetic mutants and suppression of vasorelaxation mediated by RGS2 D40Y by a PKG inhibitor.

174 ng of HCO(3)(-) adjusts endothelium-mediated vasorelaxation, microvascular perfusion, and blood press

175 diated, light-activated molecular switch for vasorelaxation might be harnessed for therapy in disease

176 ectively judged by the acetylcholine-induced vasorelaxation, NO production, angiogenic competence, an

177 creased, and nitric oxide (( *)NO)-dependent vasorelaxation of aortic ring segments was severely impa

178 lts were obtained when endothelial-dependent vasorelaxation of freshly isolated mouse aorta was used

179 Moreover, vasorelaxation of ischemic-reperfused left anterior desc

180 Administration of NPR-C agonists promotes a vasorelaxation of isolated resistance arteries and a red

181 tion range with a portable blue LED leads to vasorelaxation of porcine coronary arterial rings, a pro

182 artery, VX-445 induced a paxilline-sensitive vasorelaxation of preconstricted arteries.

183 cells, resulting in reduced estrogen-induced vasorelaxation of rat aorta.

184 (i) vasorelaxation of rat mesenteric arteries in response to

185 reaction resulted in endothelium-independent vasorelaxation of rat thoracic aorta, with an EC50 value

186 nounced enhancement in endothelial-dependent vasorelaxation of thoracic aortas and in endothelial pro

187 teries and facilitates endothelium-dependent vasorelaxation only when CO(2)/HCO(3)(-) is present.

188 gradual but profound concentration-dependent vasorelaxation over time, which was highly amplified by

189 itroprusside-induced endothelium-independent vasorelaxation (P < 0.0001).

190 Anandamide caused potent vasorelaxations (pD(2) = 6.24 +/- 0.06; R(max) = 89.4 +/

191 -dependent increase in acetylcholine-induced vasorelaxation, preventable by inhibiting NO synthase.

192 ptides maintaining the renal but lacking the vasorelaxation properties of BNP provide an alternative

193 The vasorelaxation properties seemed to be endothelium depen

194 dramatically impaired acetylcholine-induced vasorelaxation, reduced NO levels and increased ROS prod

195 +/- mice have impaired endothelium-dependent vasorelaxation, reduced vascular NO levels, and are hype

196 Neflamapimod-evoked vasorelaxation remained unaltered by the inhibition of s

197 Total GSH content of aortic tissue, vasorelaxation response of aortic rings to exogenous ONO

198 PVAT on female vessels confirmed the reduced vasorelaxation response to cromakalim associated with ma

199 mumol/g in control, P < .01), attenuated the vasorelaxation response to ONOO- (40 +/- 4.1% versus 76

200 ment of mice with simvastatin attenuates the vasorelaxation response to the beta-adrenergic agonist i

201 Contrary to our hypothesis, vasorelaxation responses to BK and sodium nitroprusside

202 Vasoconstrictor and vasorelaxation responses were measured.

203 ly attenuated impaired endothelium-dependent vasorelaxation, SERCA oxidation, ER stress, and atherosc

204 functions of hydrogen sulfide (H2S) include vasorelaxation, stimulation of cellular bioenergetics, a

205 In cirrhotic livers, NTG induced less vasorelaxation than SNAP (P <.0001).

206 the abnormal thrombosis, atherogenesis, and vasorelaxation that are characteristic of these mice.

207 mice display impaired endothelium-dependent vasorelaxation that is associated with vascular remodeli

208 The activation of PKGI by cGAMP mediates vasorelaxation that is dependent on the activity of MRP1

209 lial Cav1 and impaired endothelium-dependent vasorelaxation that was rescued by overexpressing Cav1.

210 HSP20 may regulate vasorelaxation through a direct interaction with specifi

211 Vasorelaxation to 10(-6.5) mol/L bradykinin was reduced

212 s showed that diabetes-induced impairment of vasorelaxation to acetylcholine was correlated with incr

213 on measured by blunted endothelium-dependent vasorelaxation to acetylcholine, which was normalized by

214 on measured by blunted endothelium-dependent vasorelaxation to acetylcholine, which was normalized by

215 palmitoleic acid (50 microM) did not affect vasorelaxation to anandamide.

216 Maximal endothelium-dependent vasorelaxation to BK (bradykinin; 10(-)(6)-10(-)(10) M)

217 ntly more nitric oxide and exhibited greater vasorelaxation to both calcium ionophore and acetylcholi

218 Coronary vasorelaxation to bradykinin (10(-10.5) to 10(-6.5) mol/

219 hypercholesterolemic rabbits), restored the vasorelaxation to ONOO- (61 +/- 2%, P < .01), increased

220 igh vascular BH4 was associated with greater vasorelaxations to acetylcholine (P<0.05), whereas high

221 Vasorelaxations to BNP and ACh were assessed in rings in

222 ne of aortic Sirt1 and endothelium-dependent vasorelaxation, triggered by high-fat diet feeding.

223 tivation of vascular smooth muscle cells and vasorelaxation via ETB receptor activation of endothelia

224 ation, sustained in vitro tube formation and vasorelaxation via the nitric oxide pathway.

225 The impaired vasorelaxation was a result of a decrease in both NO-med

226 Similar vasorelaxation was elicited with the additional arginase

227 Vasorelaxation was examined both in conduit and resistan

228 Vasorelaxation was examined in arteries in vitro 12-16 w

229 sis revealed that BK-induced coronary artery vasorelaxation was greater (P<0.05) after (87+/-6%) vers

230 However, vasorelaxation was impaired during hypoxia in the corona

231 Endothelium-dependent vasorelaxation was impaired in iron-loaded mice, indicat

232 Endothelium-dependent vasorelaxation was impaired in young and old JunD(-/-) m

233 Endothelium-dependent vasorelaxation was maximal with acetylocholine (ACH, 100

234 tion of Dkk3 on BP and endothelium-dependent vasorelaxation was mediated by VEGF-stimulated phosphati

235 e (eNOS) in regulating endothelium-dependent vasorelaxation, we investigated the effects of high-dens

236 d beta(2)-receptors to isoproterenol-induced vasorelaxation were found when vessels from KO mice were

237 helium-dependent and endothelium-independent vasorelaxation were measured in aortas of wild-type mice

238 Both beta-blocker-induced vasorelaxations were in the micromolar concentration ran

239 nd in vitro, inhibited endothelium-dependent vasorelaxation, whereas unmodified albumin did not.

240 endothelium-dependent, acetylcholine-induced vasorelaxation while NO-dependent smooth muscle relaxati

241 d a marked decrease in endothelium-dependent vasorelaxation, while Abca1(-/-) mice had a milder defec

242 Restoration of vasorelaxation with PEG-SOD or allopurinol suggests that

243 SNO-RBCs or NO-treated Hb induced vasorelaxation, with no differences between beta93C and