ライフサイエンスコーパス: vasoconstrictor

1 n the production of angiotensin II, a potent vasoconstrictor.

2 ular vasopressin V1 receptors, as a systemic vasoconstrictor.

3 hepatorenal syndrome consists of albumin and vasoconstrictor.

4 esponse to vasodilators and hyperresponse to vasoconstrictors.

5 S-TRPC6 in controlling vessel contraction by vasoconstrictors.

6 ch reduces vascular tone and the response to vasoconstrictors.

7 al mechanism for regulating vascular tone by vasoconstrictors.

8 a major component of mesangial responses to vasoconstrictors.

9 ve major effects on Kv channel modulation by vasoconstrictors.

10 on reflects an imbalance of vasodilators and vasoconstrictors.

11 ntraction can be altered by vasodilators and vasoconstrictors.

12 cardiac outputs necessitating greater use of vasoconstrictors.

13 displayed contractile ability in response to vasoconstrictors.

14 brane potential and an augmented response to vasoconstrictors.

15 brane potential and an augmented response to vasoconstrictors.

16 de synthase 1 restores the responsiveness to vasoconstrictors.

17 hase 1 blockade in the hyporesponsiveness to vasoconstrictors.

18 zed by hypotension and hyporesponsiveness to vasoconstrictors.

19 by the cytochrome P450 enzyme to produce the vasoconstrictor 20-hydroxyeicosatetraenoic acid (20-HETE

20 be achieved by increasing production of the vasoconstrictor, 20-hydroxyeicosatetraenoic acid in the

21 statin markedly diminished the fetal femoral vasoconstrictor (5.1 +/- 0.9 vs. 2.5 +/- 0.5 mmHg (ml mi

22 e and five minutes after topical exposure to vasoconstrictors (50 mM KCl and 20 nM Endothelin-1).

23 ous proton pump inhibitor therapy in lieu of vasoconstrictors achieved similar hemostatic effects wit

24 rachidonoylglycerol release can modulate its vasoconstrictor action in vascular tissue.

25 The vasoconstrictor action of exogenous low-dose vasopressin

26 Consistent with the dual vasodilator/vasoconstrictor action of extracellular K(+) ([K(+)](o))

27 oses of vasopressin had a very heterogeneous vasoconstrictor action; although there was no significan

28 one vasopressin to mediate its physiological vasoconstrictor actions and evidence that neuronal Kv7 c

29 ent a novel interaction between two distinct vasoconstrictor-activated TRPC channels expressed in the

30 slinked) peptide derivatives with suppressed vasoconstrictor activity and increased stability.

31 2)-responsive transducers of vasodilator and vasoconstrictor activity in lungs and tissues by regulat

32 from vascular endothelial cells, with potent vasoconstrictor activity.

33 e in CBF by decreasing P aCO 2 and enhancing vasoconstrictor activity.

34 The prospect of a non-vasoconstrictor acute migraine therapy offers a real opp

35 Serotonin is the main coronary vasoconstrictor after stenting, and thromboxane and TNFa

36 or, or withdrawal of, conventional inotropic vasoconstrictor agents (i.e., dopamine and norepinephrin

37 d by various physiological stimuli including vasoconstrictor agents such as noradrenaline, depletion

38 arteries show accentuated responsiveness to vasoconstrictor agonists in hypertension, and this abnor

39 In combination with vasoconstrictors, albumin is useful in the management of

40 As both a vasoconstrictor and a proinflammatory mediator, angioten

41 ce, including cerebral atrophy, and enhanced vasoconstrictor and blunted vasodilatory pathways.

42 At least 5 days after surgery, pressor, vasoconstrictor and cardiac chronotropic responses to ex

43 Endothelin-1 (ET-1) is a potent vasoconstrictor and co-mitogen for vascular smooth muscl

44 While individual vasoconstrictor and dilator genes have been identified,

45 antly less hypotension and no impairments in vasoconstrictor and endothelium-dependent vasodilator re

46 P antagonism markedly diminished the femoral vasoconstrictor and glycaemic responses to hypoxaemia, a

47 Critical events for vasoconstrictor and growth factor signal transduction in

48 Endothelin-1 (ET-1) is a potent vasoconstrictor and growth-promoting mediator that is in

49 It is a powerful vasoconstrictor and has structural similarities with oth

50 cular wall and CB(1)R activation reduces the vasoconstrictor and hypertensive effects of Ang II.

51 Endothelin-1 (ET-1) has potent vasoconstrictor and hypertrophic actions.

52 The practice of using vasoconstrictor and intravenous albumin therapy for the

53 to 20-hydroxyeicosatetraenoic acid, a renal vasoconstrictor and natriuretic.

54 limits the deleterious actions of TxA(2), a vasoconstrictor and platelet activator.

55 f which ET-1 is the most powerful endogenous vasoconstrictor and the predominant isoform in the cardi

56 CO has been shown to function as both a vasoconstrictor and vasodilator; however, factors that d

57 Vasoconstrictor and vasorelaxation responses were measur

58 and L-type channel activation in response to vasoconstrictors and enhance pulmonary vasoreactivity in

59 displayed contractile ability in response to vasoconstrictors and invested perivascular regions in vi

60 Vasoconstrictors and mechanical stress induce remodellin

61 Endothelin (ET-1) is one of the most potent vasoconstrictors and plays a seminal role in the pathoge

62 Endothelins are potent vasoconstrictors and signaling molecules.

63 Objective: To quantify the release of vasoconstrictors and to determine the efficacy of corona

64 also correlates with hyper-responsiveness to vasoconstrictors and vascular stiffening.

65 genes resulted in the misexpression of both vasoconstrictors and vasodilators in multiple pathways t

66 d activation of inflammatory, pro-oxidative, vasoconstrictor, and profibrotic pathways may contribute

67 ensin I to angiotensin II (Ang II), a potent vasoconstrictor, and proteolytic inactivation of bradyki

68 with acute EVH, band ligation, pharmacologic vasoconstrictors, and antibiotics are effective; notably

69 ing mice were hypocontractile in response to vasoconstrictors, and relaxation responses were unimpair

70 xhibited blunted blood pressure responses to vasoconstrictors, and their aortic, femoral, and mesente

71 hese data imply that elevations of the known vasoconstrictor Ang II in the fetal circulation may inde

72 The vasoconstrictor angiotensin II (Ang II) accelerates athe

73 ng enzyme, which catalyses production of the vasoconstrictor angiotensin II was not altered.

74 otensin-converting enzyme (ACE) produces the vasoconstrictor angiotensin II.

75 ongly impacts the functional capacity of the vasoconstrictor angiotensin II.

76 tested the hypothesis that a non-adrenergic vasoconstrictor, angiotensin II (AngII), would be less s

77 h catalyses the production of another potent vasoconstrictor, angiotensin II; and we scored the sever

78 enomedullin and suppressed the expression of vasoconstrictor angiotensinogen.

79 Future non-vasoconstrictor approaches include calcitonin gene-relat

80 likely mediated by suppressing levels of the vasoconstrictor arachidonic acid metabolite, 20-hydroxy

81 Vasoconstrictors are useful bridging therapies in HRS.

82 isolated perfused skin models), and in vivo (vasoconstrictor assay, tape stripping/dermatopharmacokin

83 e purine-releasing channels permeable to the vasoconstrictor ATP and thus may play a role in the coor

84 lar smooth muscle contraction in response to vasoconstrictors by inhibiting myosin phosphatase (MLCP)

85 ted during the actions of growth factors and vasoconstrictors can modulate disease processes by affec

86 ults support our hypothesis and suggest that vasoconstrictor capability is a contributor to orthostat

87 Endothelin-1, an extremely potent vasoconstrictor capable of increasing myometrial smooth

88 Among the vasoconstrictor challenges, only NE ameliorated the decr

89 nd reduced hypertensive responses to several vasoconstrictors, compared with wild-type mice, confirmi

90 ents with insufficient release of endogenous vasoconstrictors continue to be explored.

91 ther maintained renal vascular reactivity to vasoconstrictors contributes to the decrease in renal bl

92 , suggesting an age-related shift toward COX vasoconstrictors contributing to basal cutaneous vasomot

93 latory control or a downstream site is under vasoconstrictor control.

94 oxidative regulation of Ca(2+) influx where vasoconstrictors coupled to NAPDH oxidase (eg, angiotens

95 finger vasoconstriction that is mediated by vasoconstrictor COX products in young men, but evokes no

96 drome reversal was significantly affected by vasoconstrictor dose or type, treatment duration, age, b

97 oavailability and/or increased production of vasoconstrictors (e.g. endothelin-1).

98 However, vasoconstrictors (e.g. uridine triphosphate (UTP)) and g

99 -induced hepatic ischemia and recruitment of vasoconstrictors (e.g., endothelin-1; Edn1) leads to cle

100 rtial agonist with a preferential splanchnic vasoconstrictor effect (FE 204038) in rats with cirrhosi

101 ng O2050, a neutral antagonist, enhanced the vasoconstrictor effect of Ang II in wild type but not in

102 nsiveness to phenylephrine and increases the vasoconstrictor effect of norepinephrine and phenylephri

103 ocannabinoid formation, which attenuates its vasoconstrictor effect, suggesting that endocannabinoid

104 t beta-adrenergic vasodilatation offsets the vasoconstrictor effects of alpha-adrenergic vasoconstric

105 e properties are essential to counteract the vasoconstrictor effects of concurrent increases in muscl

106 monary arterial hypertension by blocking the vasoconstrictor effects of endothelin-A while maintainin

107 ysfunction in obesity, in addition to direct vasoconstrictor effects of endothelin.

108 chyphylaxis) is a particular problem for the vasoconstrictor effects of medications containing oxymet

109 hich is important in view of the therapeutic vasoconstrictor effects of this drug and the varied biol

110 eceptors might provide treatment without the vasoconstrictor effects of triptans.

111 r stimulation and respiratory drive, but its vasoconstrictor effects on muscle vasculature are largel

112 o not consume NO, have substantially reduced vasoconstrictor effects.

113 On isolated arteries ELDP lacked direct vasoconstrictor effects.

114 In these mice, infusion of vasoconstrictors (either endothelin 2 or angiotensin 2)

115 is required for cGMP-mediated inhibition of vasoconstrictor-elicited phospholipase Cbeta activation,

116 ure of microvascular density) and the potent vasoconstrictor endothelin 1 (EDN1); we assayed the acti

117 periovulatory rise in the expression of the vasoconstrictor endothelin 2 by follicle cells of wild-t

118 orrelate with increased levels of the potent vasoconstrictor endothelin-1 (ET-1) and PHT.

119 tal growth factor induces the release of the vasoconstrictor endothelin-1 (ET-1) from pulmonary micro

120 ion channel activated by the potent coronary vasoconstrictor endothelin-1 (ET-1) in freshly dispersed

121 We investigated whether the potent vasoconstrictor endothelin-1 (ET-1) is involved.

122 l as a 56% greater VECPE of the potent local vasoconstrictor endothelin-1 (P = 0.05) than normal-weig

123 signaling pathways regulate secretion of the vasoconstrictor endothelin-1 in endothelium.

124 oxia-independent expression of the pulmonary vasoconstrictor endothelin-1 in pulmonary endothelial ce

125 ngs by Khodorova et al. demonstrate that the vasoconstrictor endothelin-1 plays an important role in

126 , produced by intracerebral injection of the vasoconstrictor endothelin-1, on neurogenesis in the adu

127 in mice stimulates production of the potent vasoconstrictor endothelin-1, producing pulmonary hypert

128 genes-including the hyaluron receptor CD44, vasoconstrictor endothelin-1, smooth muscle growth facto

129 ues, cleaves 'big endothelin' to produce the vasoconstrictor endothelin-1.

130 ted positively with the concentration of the vasoconstrictor, endothelin 1 (P = 0.0005), and negative

131 tension (PHT) by inducing the release of the vasoconstrictor, endothelin-1.

132 blood flow by modulating the release of the vasoconstrictor, endothelin-1.

133 w that PlGF-induced expression of the potent vasoconstrictor ET-1 and its cognate ET-BR receptor occu

134 stimulating MAPK-dependent secretion of the vasoconstrictor ET-1.

135 of cyclo-oxygenase (COX-1 and COX-2)-derived vasoconstrictor factors and endothelial activation may c

136 tem activity, particularly the discharges of vasoconstrictor fibres.

137 Consistent with ATP serving as a vasoconstrictor for the pericyte-containing microvascula

138 safety of terlipressin, a systemic arterial vasoconstrictor, for cirrhosis type 1 HRS.

139 a uric acid and suppressed the fetal femoral vasoconstrictor, glycaemic and lactate acidaemic respons

140 Endothelin-1 (ET-1), a potent vasoconstrictor, has been implicated in the pathogenesis

141 to albumin, such as artificial colloids and vasoconstrictors, have been widely investigated.

142 nd increased levels of its main effector and vasoconstrictor hormone angiotensin II (Ang II).

143 idney by up-regulating the production of the vasoconstrictor hormone angiotensin II (AngII), which in

144 for NAADP-dependent Ca(2+) signaling by the vasoconstrictor hormone, endothelin-1.

145 ium dependent and thus could be activated by vasoconstrictor hormones.

146 tudies indicate that most of these cells are vasoconstrictor in function.

147 ve acute anti-migraine strategy and is a non-vasoconstrictor in terms of the mechanism of action.

148 caffeine did not modify vascular response to vasoconstrictors in splanchnic, hepatic, and collateral

149 eased systemic blood pressure in response to vasoconstrictors in spontaneously hypertensive rats.

150 ing vasodilatation and hyporesponsiveness to vasoconstrictors in the splanchnic vascular bed, with se

151 ted by protein kinase C (PKC) in response to vasoconstrictors in vascular smooth muscle cells.

152 asma levels of endothelin-1 (ET-1), a potent vasoconstrictor, in sickle cell disease (SCD).

153 Myocyte KV currents are inhibited by vasoconstrictors, including angiotensin II (Ang II), but

154 Vasoconstrictors, including endothelin-1 (ET-1), inhibit

155 d to investigate whether TRPC1 takes part in vasoconstrictor-induced mesangial contraction by mediati

156 Endothelin (ET)-1, a potent endogenous vasoconstrictor, inducer of fibrosis, and vascular smoot

157 Vasoconstrictors inhibit KV currents, but the isoform se

158 We describe a unique mechanism by which a vasoconstrictor inhibits BK channels and identify Rab11A

159 The calcium surge associated with vasoconstrictor initiated contraction also activates a c

160 icant regional heterogeneity in the specific vasoconstrictor involved.

161 cirrhosis, but current therapy with systemic vasoconstrictors is ineffective in a substantial proport

162 trictor-like (MVC(like), 39%) from cutaneous vasoconstrictor-like (CVC(like), 28%) SPNs.

163 eflex, allowing the discrimination of muscle vasoconstrictor-like (MVC(like), 39%) from cutaneous vas

164 hanol failed to modify Ca(2+) waves, a major vasoconstrictor mechanism.

165 during labor and delivery from a reliance on vasoconstrictor mechanisms to those promoting NO-depende

166 ng the idea that O2 -dependent production of vasoconstrictors mediates arteriolar O2 reactivity, with

167 changes in blood pressure and suggest that a vasoconstrictor metabolite of COX-1 could play a role in

168 nstrates the important role of COX-1 derived vasoconstrictor metabolites in regulation of microvascul

169 suggests an important role of COX-1 derived vasoconstrictor metabolites in the regulation of microva

170 are partially due to increased expression of vasoconstrictor molecule endothelin 1 and a concomitant

171 Muscle sympathetic vasoconstrictor nerve activity increases with advancing

172 current line of thinking, whether cutaneous vasoconstrictor neural activity is enhanced and capable

173 licate in vivo recordings of EPSPs in muscle vasoconstrictor neurons, produced a 2.4-fold amplificati

174 wed that neuropeptide Y (NPY), a sympathetic vasoconstrictor neurotransmitter, stimulates endothelial

175 operties following iontophoresis of a potent vasoconstrictor, noradrenaline.

176 x control of both heart rate and sympathetic vasoconstrictor outflow to higher pressures, resulting i

177 reflex control of heart rate and sympathetic vasoconstrictor outflow to higher pressures, without cha

178 es not affect arterial pressure, sympathetic vasoconstrictor outflow, or baroreflex gain.

179 The vasoconstrictor peptide endothelin-1 (ET-1) is a transcr

180 Plasma concentrations of the vasoconstrictor peptide endothelin-1 are increased in pa

181 urthermore, COX-2 expression, induced by the vasoconstrictor peptide ET-1 or the cytokine interleukin

182 Endothelin 1 (ET-1), a potent vasoconstrictor peptide expressed by endothelium, is als

183 Although endothelin-1 (ET-1) is a potent vasoconstrictor peptide implicated in several retinal pa

184 Endothelin-1 (ET-1) is a potent vasoconstrictor peptide with mitogenic actions linked to

185 of PGs would increase hyperaemia by blocking vasoconstrictor PGs.

186 perfusion pressure was manipulated with the vasoconstrictor phenylephrine.

187 Pretreatment with a vasoconstrictor, phenylephrine, resulted in a reversal o

188 enging of host amines would antagonize their vasoconstrictor, platelet-aggregating, and pain-inducing

189 Endothelin-1, a potent vasoconstrictor, plays an important role in pulmonary hy

190 ed one or two cartridges of local anesthetic/vasoconstrictor prior to dental treatment.

191 -inflammatory drugs) or specific agents with vasoconstrictor properties (ie, triptans or ergot deriva

192 e cells and by an EDCF that is principally a vasoconstrictor prostaglandin generated by COX-2 >-1 act

193 f cyclo-oxygenases (COX-1 and COX-2) and the vasoconstrictor prostaglandins, thromboxane A2 (TXA2 ) a

194 lly prolonged signaling by G protein-coupled vasoconstrictor receptors can contribute to the onset of

195 axiK channels are linked to counterbalancing vasoconstrictor receptors is unknown.

196 Whether vasoconstrictors regulate the multisubunit composition o

197 Plasma endothelin-1 (pg/mL), an important vasoconstrictor regulated by NF-kappaB, increased from 2

198 rker of endothelial dysfunction, is a potent vasoconstrictor released by endothelial cells and an imp

199 Vasoconstrictor reserve therefore may be one mechanism u

200 e synthesis and contribute to the attenuated vasoconstrictor response in aged skin.

201 und 48/80 in PAR-2(+/+) mice and ablated the vasoconstrictor response in PAR-2(-/-) mice.

202 pt sarcolemmal targeting of nNOSmu, with the vasoconstrictor response measured as a decrease in muscl

203 Total cutaneous vasoconstrictor response score to topical beclometasone

204 obe, norepinephrine induced a dose-dependent vasoconstrictor response that was not significantly alte

205 itters mediated a significant portion of the vasoconstrictor response to cold stress in HTN.

206 sympathetic co-transmitters in mediating the vasoconstrictor response to cold stress in hypertension.

207 ertension increases the peripheral cutaneous vasoconstrictor response to cold via greater increases i

208 dase (XO) contribute to the fetal peripheral vasoconstrictor response to hypoxia via interaction with

209 NMMA in all subjects (P<0.001); however, the vasoconstrictor response to L-NMMA was greater (P=0.04)

210 ous work indicates that at least part of the vasoconstrictor response to LC may be through an inhibit

211 ystemic hypotension, a significantly blunted vasoconstrictor response to norepinephrine, and an impai

212 ested the hypothesis that the enhanced renal vasoconstrictor response to renal nerve stimulation in C

213 The renal vasoconstrictor response to renal nerve stimulation is g

214 Cutaneous vasoconstrictor response to topical beclometasone, airwa

215 rogen causes vasodilation and attenuates the vasoconstrictor response to various stimuli, including h

216 to adrenergic stimuli to the impaired reflex vasoconstrictor response to whole-body cooling in human

217 g acute hypoxia opposes the fetal peripheral vasoconstrictor response, part of the brain-sparing defe

218 e but not in PAR-2(-/-) mice, which showed a vasoconstrictor response.

219 c arteries and veins will exhibit diminished vasoconstrictor responses after spaceflight.

220 rom patients with advanced cirrhosis impairs vasoconstrictor responses and decreases blood pressure,

221 holysis, calculated as the difference in the vasoconstrictor responses during adenosine infusion and

222 , and 12 (57%) patients (group B) had normal vasoconstrictor responses during LBNP (FVR increased by

223 Forearm vasoconstrictor responses during low dose adenosine (-38

224 In contrast, vasoconstrictor responses during moderate (-22 +/- 6%) a

225 a presynaptic facilitatory influence on the vasoconstrictor responses evoked by bursts at high frequ

226 inversely with the magnitude of sympathetic vasoconstrictor responses in contracting hindlimbs.

227 To test these hypotheses, we measured vasoconstrictor responses in the forearms of pre- and po

228 se changes in baseline vascular conductance, vasoconstrictor responses in the leg to phenylephrine an

229 responses in vitro and exaggerated pulmonary vasoconstrictor responses in vivo and are defective in o

230 In the fetal placenta, the overall in vivo vasoconstrictor responses of the blood vessels to Ang II

231 ociated with impaired vasodilator as well as vasoconstrictor responses to a wide range of stimuli.

232 Similarly, vasoconstrictor responses to alpha(2)-receptor stimulati

233 Despite the lower BP, acute vasoconstrictor responses to Ang II in the systemic vasc

234 Patients with RP had abnormal vasoconstrictor responses to cold pressor tests (CPT) th

235 Finally, in five subjects the forearm vasoconstrictor responses to direct alpha 1-adrenergic (

236 Forearm vasoconstrictor responses to direct alpha(1)-receptor st

237 During adenosine, forearm vasoconstrictor responses to direct alpha(1)-stimulation

238 hat adenosine triphosphate (ATP) can inhibit vasoconstrictor responses to endogenous noradrenaline re

239 ng acute hypoxaemia offsets fetal peripheral vasoconstrictor responses to hypoxaemia via chemoreflex

240 After 1 month of treatment, vasoconstrictor responses to intra-arterial norepinephri

241 Systemic and renal vasoconstrictor responses to L-NAME were also similar in

242 Whole-leg vasoconstrictor responses to local intrafemoral artery i

243 Vasoconstrictor responses to phenylephrine and serotonin

244 Vasoconstrictor responses to sympathetic nerve stimulati

245 In protocol 2, forearm vasoconstrictor responses to the high dose of tyramine w

246 We hypothesized that vasoconstrictor responses to three manoeuvres (neck pres

247 In young men, the vasoconstrictor responses to tyramine (-25 +/- 1 versus

248 Maximal vasoconstrictor responses to tyramine (-30 +/- 3 versus

249 The magnitude of the blunted vasoconstrictor responses was similar for both receptor

250 Vasoconstrictor responses were evoked in arteries via no

251 Contrary to that hypothesized, myogenic vasoconstrictor responses were lower and vascular disten

252 In NTG-treated rats, vasoconstrictor responses were similar at rest, but were

253 tribute to the regulation of vasodilator and vasoconstrictor responses, and their activity is regulat

254 cellular mechanisms underlying Ang II-evoked vasoconstrictor responses.

255 Leg sympathetic vasoconstrictor responsiveness (reduction in leg vascula

256 muscles does not explain blunted sympathetic vasoconstrictor responsiveness during endotoxemia.

257 othesis that postjunctional alpha-adrenergic vasoconstrictor responsiveness is reduced in the leg cir

258 aluated whether apparent loss of sympathetic vasoconstrictor responsiveness relates to distended smoo

259 te (ATP) has been shown to blunt sympathetic vasoconstrictor responsiveness similar to exercise.

260 bursts min(-1), and was inversely related to vasoconstrictor responsiveness to both NA (r = 0.61, P =

261 at post-junctional alpha-adrenergic receptor vasoconstrictor responsiveness to endogenous noradrenali

262 At each dose of SNP, cutaneous vasoconstrictor responsiveness was assessed during a 3 m

263 hypoxia and endotoxemia blunted sympathetic vasoconstrictor responsiveness.

264 Enhanced vasoconstrictor sensitivity and elevations in soluble fm

265 may be the primary event leading to enhanced vasoconstrictor sensitivity that is characteristic of pr

266 inhibit G protein-coupled receptor-mediated vasoconstrictor signaling.

267 oxygen species, in conjunction with elevated vasoconstrictor signalling via endothelin-1, reduces the

268 We show that RGS2 regulates vasoconstrictor-stimulated Ca(2+) store release, capacit

269 We show that angiotensin II (Ang II), a vasoconstrictor, stimulates degradation of KV 1.5, but n

270 e sympathetic nerve activity and circulating vasoconstrictor substances during exercise.

271 These data suggest that the cutaneous vasoconstrictor system is engaged and is capable of decr

272 as indicated by more marked activity of the vasoconstrictor systems.

273 rms included: hepatorenal syndrome; albumin; vasoconstrictor; terlipressin; midodrine; octreotide; no

274 Angiotensin II (Ang II) is a potent vasoconstrictor that increases concomitant with sFlt-1 d

275 ete a substance known as palytoxin, a potent vasoconstrictor that inhibits the membranous sodium-pota

276 Endothelin-2 (EDN2) is a potent vasoconstrictor that is transiently produced prior to fo

277 lin-1 (ET-1) is a potent endothelial-derived vasoconstrictor that may modulate cholinergic cutaneous

278 Vasoconstrictors that bind to phospholipase C-coupled re

279 r aspiration of thrombi and thrombus-derived vasoconstrictor, thrombogenic, and inflammatory substanc

280 ocal anesthetic solutions frequently contain vasoconstrictors to increase the depth and/or duration o

281 ght help explain the greater skeletal muscle vasoconstrictor tone and reduced blood flow during large

282 age, but does not result in elevated forearm vasoconstrictor tone because of a selective reduction in

283 and assessed its influence on ET-1-dependent vasoconstrictor tone in obesity.

284 hat older healthy humans demonstrate greater vasoconstrictor tone in their active muscles during exer

285 However, endothelin-1-mediated vasoconstrictor tone increases with age and contributes

286 We conclude that coronary vasoconstrictor tone is greater in men than women during

287 tors to offset the transduction of MSNA into vasoconstrictor tone was lost in postmenopausal women.

288 tensive blacks have enhanced ET(A)-dependent vasoconstrictor tone, probably related to increased prod

289 acterized by increased endothelin-1-mediated vasoconstrictor tone.

290 We propose that vasoconstrictor TP receptor and MaxiK-channel direct int

291 a decreased hypertensive response following vasoconstrictor treatment.

292 o promote vascular relaxation by attenuating vasoconstrictor-triggered Ca2+ signaling in vascular smo

293 versus 7.5%), inotrope (39% versus 50%) and vasoconstrictor usage (66% versus 64%) were not differen

294 nT, ECG changes, cardiac index, inotrope and vasoconstrictor use, renal dysfunction, and lung injury.

295 creasing renal blood flow through the use of vasoconstrictors (vasopressin, norepinephrine) in combin

296 atorenal syndrome treatment with albumin and vasoconstrictor were sought.

297 y; their effects on the vascular response to vasoconstrictors were examined in vitro and in vivo.

298 Levels of endothelin-1 (ET-1), a potent vasoconstrictor, were affected by both RhoGDI2 reconstit

299 Angiotensin II (Ang II) is a potent vasoconstrictor with an important role in controlling bl

300 results from the enhanced effect of several vasoconstrictors with an effect size sequence of adenosi