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 de synthase 1 restores the responsiveness to vasoconstrictors.

5 hase 1 blockade in the hyporesponsiveness to vasoconstrictors.

6 zed by hypotension and hyporesponsiveness to vasoconstrictors.

7 esponse to vasodilators and hyperresponse to vasoconstrictors.

8 S-TRPC6 in controlling vessel contraction by vasoconstrictors.

9 al mechanism for regulating vascular tone by vasoconstrictors.

10 a major component of mesangial responses to vasoconstrictors.

11 ve major effects on Kv channel modulation by vasoconstrictors.

12 on reflects an imbalance of vasodilators and vasoconstrictors.

13 ch reduces vascular tone and the response to vasoconstrictors.

14 ntraction can be altered by vasodilators and vasoconstrictors.

15 cardiac outputs necessitating greater use of vasoconstrictors.

16 displayed contractile ability in response to vasoconstrictors.

17 brane potential and an augmented response to vasoconstrictors.

18 brane potential and an augmented response 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 ex resetting promotes heightened sympathetic vasoconstrictor activity and maintains blood pressure st

32 tation appears to favour a lower sympathetic vasoconstrictor activity compared to Lowlanders for bloo

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

34 from vascular endothelial cells, with potent vasoconstrictor activity.

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

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

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

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

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

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

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

42 As both a vasoconstrictor and a proinflammatory mediator, angioten

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

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

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

46 While individual vasoconstrictor and dilator genes have been identified,

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

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

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 spring vascular function in response to both vasoconstrictors and dilators.

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

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

61 Vasoconstrictors and mechanical stress induce remodellin

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

63 Endothelins are potent vasoconstrictors and signaling molecules.

64 retinal venular responsiveness to endogenous vasoconstrictors and the contribution of the reverse-mod

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

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

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

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

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

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

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

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

73 The vasoconstrictor angiotensin II (Ang II) accelerates athe

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

75 nt conversion of angiotensin I to the potent vasoconstrictor angiotensin II while simultaneously halt

76 (ACE) converts angiotensin I into the potent vasoconstrictor angiotensin II, which regulates blood pr

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

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

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

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

81 enomedullin and suppressed the expression of vasoconstrictor angiotensinogen.

82 Future non-vasoconstrictor approaches include calcitonin gene-relat

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

84 Vasoconstrictors are useful bridging therapies in HRS.

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

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

87 ance retinal venular responses to endogenous vasoconstrictors by activating reverse-mode NCX.

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

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

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

91 Among the vasoconstrictor challenges, only NE ameliorated the decr

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

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

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

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

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

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

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

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

100 -fold, and urotensin-II, the strongest known vasoconstrictor, doubled.

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

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

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

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

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

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

107 sed probably due to a predominantly systemic vasoconstrictor effect of terlipressin.

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

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

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

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

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

113 Ursodeoxycholic acid inhibits uptake and vasoconstrictor effects of taurocholate in human placent

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

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

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

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

118 On isolated arteries ELDP lacked direct vasoconstrictor effects.

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

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

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

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

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

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

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

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

127 n deficiency and increased expression of the vasoconstrictor endothelin-1 (ET-1) within PASMCs.

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

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

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

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

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

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

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

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

136 ated EGFR promotes the secretion of a potent vasoconstrictor, endothelin-1 (EDN1), which continues to

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

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

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

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

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

142 tem activity, particularly the discharges of vasoconstrictor fibres.

143 as utilized to induce a range of sympathetic vasoconstrictor firing while measuring beat-by-beat bloo

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

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

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

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

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

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

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

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

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

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

154 ET-1 is the most potent vasoconstrictor in the human cardiovascular system and h

155 We observe here increased responses to vasoconstrictors in arteries from Jak2V617F mice resulti

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

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

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

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

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

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

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

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

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

165 Vasoconstrictors inhibit KV currents, but the isoform se

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

167 icant regional heterogeneity in the specific vasoconstrictor involved.

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

169 Endothelin-1, a very potent vasoconstrictor, is a key modulator of blood flow and pr

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

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

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

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

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

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

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

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

178 Muscle sympathetic vasoconstrictor nerve activity increases with advancing

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

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

181 operties following iontophoresis of a potent vasoconstrictor, noradrenaline.

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

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

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

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

186 /-) mice exhibiting lower mRNA levels of the vasoconstrictor peptide ET-1 (endothelin-1) and higher l

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

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

189 ) is the precursor of one of the most potent vasoconstrictors, peptide angiotensin II.

190 of PGs would increase hyperaemia by blocking vasoconstrictor PGs.

191 perfusion pressure was manipulated with the vasoconstrictor phenylephrine.

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

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

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

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

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

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

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

199 ood, it programmed hypertension by enhancing vasoconstrictor reactivity and impairing NO-independent

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

201 Whether vasoconstrictors regulate the multisubunit composition o

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

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

204 Vasoconstrictor reserve therefore may be one mechanism u

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

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

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

208 Total cutaneous vasoconstrictor response score to topical beclometasone

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

210 FP plasmid into RGS2(-/-) MAs suppressed the vasoconstrictor response to angiotensin II.

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

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

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

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

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

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

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

218 Cutaneous vasoconstrictor response to topical beclometasone, airwa

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

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

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

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

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

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

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

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

227 Forearm vasoconstrictor responses during low dose adenosine (-38

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

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

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

231 s critical signaling cascade exaggerated the vasoconstrictor responses of cerebral and mesenteric res

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

233 2V617F MPNs are characterized by exacerbated vasoconstrictor responses resulting from increased endot

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

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

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

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

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

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

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

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

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

243 Whole-leg vasoconstrictor responses to local intrafemoral artery i

244 Vasoconstrictor responses to phenylephrine and serotonin

245 Vasoconstrictor responses to sympathetic nerve stimulati

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 Vasoconstrictor responses were evoked in arteries via no

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

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

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

253 cellular mechanisms underlying Ang II-evoked vasoconstrictor responses.

254 Leg sympathetic vasoconstrictor responsiveness (reduction in leg vascula

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

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

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

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

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

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

261 hypoxia and endotoxemia blunted sympathetic vasoconstrictor responsiveness.

262 Enhanced vasoconstrictor sensitivity and elevations in soluble fm

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

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

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

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

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

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

269 aine 2% solution (Scandicaine(R) 2%, without vasoconstrictor supplementation).

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

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

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

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

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

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

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

277 Vasoconstrictors that bind to phospholipase C-coupled re

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

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

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

281 vasodilator capacity is involved, heightened vasoconstrictor tone and/or responsiveness may also cont

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