ライフサイエンスコーパス: vasorelaxation

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

2 ced Cav1, and impaired endothelium-dependent vasorelaxation.

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

4 ochondria, leading to production of cGMP and vasorelaxation.

5 t role for phosphorylated HSP20 in mediating vasorelaxation.

6 triggering cellular activity known to induce vasorelaxation.

7 ion, thermosensation, mechanoregulation, and vasorelaxation.

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

9 l injury, and improved endothelial-dependent 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 as barium and ouabain reversed K(+)-mediated vasorelaxation.

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

16 ithout effects on contraction or NO-mediated vasorelaxation.

17 approximately 80% of acetylcholine-mediated vasorelaxation.

18 ive stress, induce angiogenesis, and promote 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 on of cytoplasmic calcium concentrations and vasorelaxation.

24 7,8-DHHD also produced vasorelaxation.

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

26 peutic strategies by targeting cell-mediated vasorelaxation.

27 ts knock-down inhibits endothelium-dependent vasorelaxation.

28 P binding, namely kinase activation and thus vasorelaxation.

29 acetylcholine-induced, nitric oxide-mediated vasorelaxation.

30 f vasoconstriction and endothelium-dependent vasorelaxation.

31 omboxane mimetic, resulted in dose-dependent vasorelaxation.

32 pressure, and impaired endothelium-dependent vasorelaxation.

33 tial for PKG activation and angiogenesis and vasorelaxation.

34 nduced vasoconstriction or carbachol-induced vasorelaxation.

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

36 ramide but failed to normalize the defect in vasorelaxation.

37 ucose utilization, and endothelium-dependent vasorelaxation.

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

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

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

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

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

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

44 This remaining vasorelaxation activity, termed endothelium-derived hype

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 Endothelium-dependent vasorelaxations and direct measurements of vascular supe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 Vasorelaxation by estrogens in female and male rat aorta

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

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

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

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

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

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

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

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

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

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

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

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

96 The vasorelaxation elicited by acetylcholine (ACh) in phenyl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 Vasorelaxation in response to acetylcholine was inhibite

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 Moreover, vasorelaxation of ischemic-reperfused left anterior desc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 Vasoconstrictor and vasorelaxation responses were measured.

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

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

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

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

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

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

179 HSP20 may regulate vasorelaxation through a direct interaction with specifi

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

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

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

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

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

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

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

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

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

189 Vasorelaxations to BNP and ACh were assessed in rings in

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

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

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

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

194 Similar vasorelaxation was elicited with the additional arginase

195 Vasorelaxation was examined both in conduit and resistan

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

197 However, vasorelaxation was impaired during hypoxia in the corona

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

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

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

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

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

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

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

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

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

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