ライフサイエンスコーパス: vasoactive

1 te its effects on neuronal activity from its vasoactive actions.

2 both MRI, MR angiography and intracavernosal vasoactive agent administration can be questioned.

3 Both MRI and intravenous vasoactive agent administration may be helpful in suspic

4 dney disease, cancer, respiratory infection, vasoactive agent use, and receipt of renal replacement t

5 ng increased neurotransmission and releasing vasoactive agents (e.g., K(+)) from perivascular endfeet

6 5]), temporary pacemaker (OR, 6.4 [2.2-19]), vasoactive agents (OR, 1.5 [1.1-2.1]), acute (<24 hours)

7 ortality rates were associated with starting vasoactive agents 1-6 hours after onset.

8 Fluids and vasoactive agents are both used to treat septic shock, b

9 As with venules, vasoactive agents can alter both the permeability and co

10 HR: 1.94 [95% CI: 1.26 to 2.98]), the use of vasoactive agents for bleeding (HR: 2.01 [95% CI: 0.91 t

11 Fluids and vasoactive agents had strong, interacting associations w

12 ever, there may be differential responses to vasoactive agents in AHF patients with reduced versus pr

13 Starting vasoactive agents in the initial hour may be detrimental

14 d flow in response to temperature changes or vasoactive agents is a feature of cardiovascular disease

15 uninvolved, skin indicates that these potent vasoactive agents may play a role in wealing and tissue

16 arterioles directly upstream in response to vasoactive agents or contraction of adjacent muscle fibr

17 , illness category, and need for intravenous vasoactive agents prior to the arrest.

18 Assessment score that takes into account all vasoactive agents used in current clinical practice, use

19 Mortality was lowest when vasoactive agents were begun 1-6 hours after onset, with

20 ascular leakage and expression of the potent vasoactive agents' calcitonin gene-related peptide (CGRP

21 significant change in the use of IV fluids, vasoactive agents, or blood products.

22 uid administration, only thereafter starting vasoactive agents, while continuing aggressive fluid adm

23 ds being given with such early initiation of vasoactive agents.

24 Thus, vasoactive agonists probably invoke unique mechanisms th

25 In this study, we examined the ability of vasoactive agonists to induce dynamic changes in vascula

26 orientation before and after treatment with vasoactive agonists.

27 ologic and inflammatory responses, including vasoactive amine sensitization (VAAS) to histamine (HA),

28 ggregation and activation through release of vasoactive amines in the inflammatory response, resultin

29 Still, histamine and other vasoactive amines remained at low levels, thus not affec

30 ptidase that converts angiotensin I into the vasoactive and aldosterone-stimulating peptide angiotens

31 ue to many factors, such as the influence of vasoactive and anesthetic drugs, total muscular relaxati

32 with ERMs, we examine here the expression of vasoactive and inflammatory mediators in the vitreous of

33 cultured PAH and control P-EC proliferation, vasoactive and proinflammatory factor production, and cr

34 r hemodynamic stabilization upon endoscopic, vasoactive, and antibiotic treatment.

35 s in patients receiving standard endoscopic, vasoactive, and antibiotic treatment.

36 d electrolyte fluid homeostasis, cleaves the vasoactive angiotensin-I, bradykinin, and a number of ot

37 trol during exercise in older adults involve vasoactive ATP, we speculate that circulating ATP is red

38 er Doppler in response to thermal stress and vasoactive challenge.

39 VEGF induced vasoactive changes in pig retinal arterioles are depende

40 the influence of bevacizumab on VEGF induced vasoactive changes on ET-1 pre-contracted vessels.

41 erivascular adipose tissue or PVAT) releases vasoactive compounds that regulate vascular smooth muscl

42 Numerous vasoactive cytokines are upregulated during sepsis, incl

43 e elaboration of reactive oxygen species and vasoactive cytokines, altering the inflammatory milieu i

44 ars, leading to the discovery of its role in vasoactive, cytoprotective and anti-inflammatory respons

45 Exclusions were receiving vasoactive drug(s) prior to hospital admission, having k

46 ability of CA in healthy older adults during vasoactive drug-induced changes in arterial pressure ass

47 Mechanical ventilation (47.9% of patients), vasoactive drugs (51.2%), and dialysis (25.9%) were asso

48 on, more patients in the HFOV group received vasoactive drugs (91% vs. 84%, P=0.01) and received them

49 nafil (P = 0.004), had a shorter duration of vasoactive drugs (P = 0.02), and less often failed treat

50 yndrome that compared the efficacy of active vasoactive drugs (terlipressin, midodrine, octreotide, n

51 Treatment with vasoactive drugs as well as antibiotic treatment is star

52 pected to require mechanical ventilation and vasoactive drugs for at least 12 hours to either tight g

53 n optimization, 92 institutions (77.3%) used vasoactive drugs to achieve a target mean arterial blood

54 clusion and its duration, length of surgery, vasoactive drugs used, blood loss, and transfusion) were

55 Vasoactive drugs were used in 23 patients (68%) and rena

56 nd resuscitation with intravenous fluids and vasoactive drugs when needed.

57 ibing order of interventions withdrawn, with vasoactive drugs withdrawn first followed by gradual wit

58 ological variables, sedativeanalgesic drugs, vasoactive drugs, and medical/surgical therapies for int

59 ated by increased use of intravenous fluids, vasoactive drugs, and red-cell transfusions and reflecte

60 Mechanical ventilation, vasoactive drugs, and renal replacement therapy were adm

61 are-associated infection, the need for other vasoactive drugs, and the multiple organ dysfunction sco

62 f vasoactivity, using a small panel of known vasoactive drugs.

63 d and beta-Ad receptor-dependent and its net vasoactive effect was concentration- and time-dependent.

64 plexus, an intervening neural structure with vasoactive effects, was not responsible for the increase

65 low (CBF) reflect neuronal activation or its vasoactive effects.

66 n of astroglial metabolism (-35%, p < 0.01), vasoactive epoxyeicosatrienoic acids (EETs; -60%, p < 0.

67 ional repertoire, which results in important vasoactive events in the pleural space.

68 ry blood flow by inert gas re-breathing, and vasoactive exchange via the Fick principle.

69 rved that vitreous concentrations of classic vasoactive factors (e.g., vascular endothelial growth fa

70 ctivated receptor gamma regulates a panel of vasoactive factors communicating between diseased pulmon

71 During exercise there is a balance between vasoactive factors that facilitate increases in blood fl

72 that adipose tissue from Adipo-MROE secrete vasoactive factors that preferentially influence vascula

73 al expression of angiogenic, fibrogenic, and vasoactive factors.

74 ic vasconstriction despite blockade of these vasoactive factors.

75 sive multiorgan dysfunction, ventilator- and vasoactive-free days at Day 28, functional status, and m

76 entilator-free days were 16 (IQR, 0-25), and vasoactive-free days were 23 (IQR, 12-28).

77 ortality (primary outcome); ventilator-free, vasoactive-free, and organ failure-free days; and length

78 The expression of an array of vasoactive genes was assessed in the thoracic aorta and

79 Calcium-dependent release of vasoactive gliotransmitters is widely assumed to trigger

80 n fraction underwent aggressive titration of vasoactive HF therapies with assessment of central aorti

81 s have highlighted angiotensin II (AngII), a vasoactive hormone, as a potent HIF-1 activator in vascu

82 has been used to suppress the production of vasoactive hormones and relieve symptoms of hormone hype

83 the glomerular filtration rate, P = 0.14, or vasoactive hormones were found.

84 fect glomerular filtration rate or levels of vasoactive hormones.

85 faximin on hemodynamics, renal function, and vasoactive hormones.

86 s ratio, 0.82; 95% CI, 0.68-0.98), and fewer vasoactive infusion days (3.0 vs 3.3 d; p < 0.001) when

87 ed mechanical ventilation (74% of patients), vasoactive infusions (55%), and corticosteroids (45%).

88 oped cardiovascular dysfunction treated with vasoactive infusions a median of 5 days after T cell the

89 acute kidney injury, and shorter duration of vasoactive infusions when compared with exclusive use of

90 the hypersecretion of insulin (5 patients), vasoactive intestinal peptide (5 patients), gastrin (2 p

91 stem cells, we found that costimulation with vasoactive intestinal peptide (V) and phorbol ester (P)

92 e in response to inhibitory neurotransmitter vasoactive intestinal peptide (VIP) and direct electrica

93 diated by the primary coupling neuropeptide, vasoactive intestinal peptide (VIP) and its canonical re

94 HMG) cells were examined for the presence of vasoactive intestinal peptide (VIP) and muscarinic acety

95 activity in the visual cortex contains both vasoactive intestinal peptide (VIP) and somatostatin (SS

96 concentration efficiency for the target drug vasoactive intestinal peptide (VIP) as conventional part

97 s from our laboratory have demonstrated that vasoactive intestinal peptide (VIP) directly converts th

98 Exogenous vasoactive intestinal peptide (VIP) down-regulates pro-i

99 Vasoactive intestinal peptide (VIP) has been widely acce

100 Drosophila is remarkably similar to that of vasoactive intestinal peptide (VIP) in mammals.

101 small proline-rich protein 1a (sprr1a), and vasoactive intestinal peptide (vip) in the trigeminal ga

102 Vasoactive intestinal peptide (VIP) induces regulatory d

103 One solution to this problem could be the vasoactive intestinal peptide (VIP) interneurons, which

104 Vasoactive intestinal peptide (VIP) is a neurotransmitte

105 Vasoactive intestinal peptide (VIP) is an acknowledged n

106 Vasoactive intestinal peptide (VIP) is an anti-inflammat

107 Vasoactive intestinal peptide (VIP) is an anti-inflammat

108 Vasoactive intestinal peptide (VIP) is more prominent in

109 Vasoactive intestinal peptide (VIP) mediates a broad ran

110 ed by sound, while visual responses of L2/L3 vasoactive intestinal peptide (VIP) neurons were suppres

111 n interneurons expressing Cre recombinase in vasoactive intestinal peptide (VIP) or parvalbumin (PV)

112 synthase (NOS), serotonin, substance P (SP), vasoactive intestinal peptide (VIP) or vesicular acetylc

113 tested the hypothesis that the neuropeptide vasoactive intestinal peptide (VIP) regulates adhesion m

114 We show that vasoactive intestinal peptide (VIP) secreted by the inne

115 ntaining choline acetyltransferase (ChAT) or vasoactive intestinal peptide (VIP) share characteristic

116 ng parvalbumin (PV), somatostatin (SST), and vasoactive intestinal peptide (VIP) show cell-type-speci

117 demonstrated their dependence upon G-coupled vasoactive intestinal peptide (VIP) signaling.

118 Vasoactive intestinal peptide (VIP) suppresses Th1 immun

119 decreased the area of nitrergic neurons and vasoactive intestinal peptide (VIP) varicosities.

120 Vasoactive Intestinal Peptide (VIP), a pulmonary vasodil

121 .5 (PGP 9.5), a general neuronal marker, and vasoactive intestinal peptide (VIP), a sudomotor nerve f

122 sion of the anti-inflammatory neuropeptides, vasoactive intestinal peptide (VIP), and pituitary adeny

123 opulations, expressing somatostatin (SOM) or vasoactive intestinal peptide (VIP), are active as popul

124 We explored the relation between vasoactive intestinal peptide (VIP), CRTH2, and eosinoph

125 t their regulation by neuropeptides, such as vasoactive intestinal peptide (VIP), during Pseudomonas

126 essing parvalbumin (PV), somatostatin (SOM), vasoactive intestinal peptide (VIP), or neuropeptide Y.

127 ntal Cell, Nedvetsky et al. (2014) find that vasoactive intestinal peptide (VIP), secreted by parasym

128 al that locomotion increases the activity of vasoactive intestinal peptide (VIP), somatostatin (SST)

129 ctionally important neuropeptides, including vasoactive intestinal peptide (VIP), which drives light

130 owever, targeting of somatostatin (SOM)- and vasoactive intestinal peptide (VIP)-expressing INs led t

131 tional ErbB4 deletion, we tested the role of vasoactive intestinal peptide (VIP)-expressing interneur

132 to light induces a gene program in cortical vasoactive intestinal peptide (VIP)-expressing neurons t

133 cuit inhibition and a subsequent increase in vasoactive intestinal peptide (VIP)-mediated disinhibiti

134 In contrast, activating vasoactive intestinal peptide (VIP)-positive interneuron

135 g animals revealed that locomotion activates vasoactive intestinal peptide (VIP)-positive neurons in

136 sitive and calretinin (Cr)-positive (but not vasoactive intestinal peptide (VIP)-positive) interneuro

137 ctly on nociceptors to induce the release of vasoactive intestinal peptide (VIP).

138 litude of pacemaking in SCN circuits lacking vasoactive intestinal peptide (VIP).

139 PEG5kDa-cholane) to a 28 amino acid peptide, vasoactive intestinal peptide (VIP).

140 originating from the SCN neurons expressing vasoactive intestinal peptide (VIP+ neurons).

141 The circadian synchronizer vasoactive intestinal peptide also stimulates ILC2 cells

142 The DeltaF508 mice overexpressed vasoactive intestinal peptide and had defects in gallbla

143 In particular, the effects of vasoactive intestinal peptide and secretin on intra-acin

144 ns of adoptively transferred N-alpha-syn and vasoactive intestinal peptide immunocytes or natural Tre

145 In SCN lacking vasoactive intestinal peptide or its receptor, mCry1 exp

146 Endogenous mediators, such as vasoactive intestinal peptide or prostaglandin E2 (PGE2)

147 yndrome, exonic duplications in the gene for vasoactive intestinal peptide receptor 2 (VIPR2), and ex

148 hat, upon agonist stimulation, a GPCR called vasoactive intestinal peptide receptor 2 (VPAC2) is shed

149 Vasoactive intestinal peptide receptor 2 can elicit immu

150 olase, agonists of natriuretic peptide A and vasoactive intestinal peptide receptor 2, and a novel mi

151 located within 89 kilobases upstream of the vasoactive intestinal peptide receptor gene VIPR2.

152 These findings implicate altered vasoactive intestinal peptide signalling in the pathogen

153 Epithelial responsiveness to vasoactive intestinal peptide was increased after enteri

154 of parvalbumin (PV), somatostatin (SST), and vasoactive intestinal peptide were decreased in hypoxic-

155 ted agonist (isoproterenol (isoprenaline) or vasoactive intestinal peptide) in the presence of HCO3-

156 Treatment with vasoactive intestinal peptide, an anti-inflammatory neur

157 rosine kinase, endothelial progenitor cells, vasoactive intestinal peptide, and miRNA in PAH therapeu

158 n mCry1 expression and its interactions with vasoactive intestinal peptide, cAMP, and PER at the hear

159 ast, interneurons containing neuropeptide Y, vasoactive intestinal peptide, or the 5-hydroxytryptamin

160 neuron-specific enolase, gastrin, glucagon, vasoactive intestinal peptide, pancreatic polypeptide, a

161 novel peptide with structural similarity to vasoactive intestinal peptide, regulates production of e

162 9.5, neuronal nitric oxide synthase (nNOS), vasoactive intestinal peptide, substance P, and tyrosine

163 and duodenal acidity, and overexpressed the vasoactive intestinal peptide-a myorelaxant factor for t

164 neurons were labeled in parvalbumin-Cre and vasoactive intestinal peptide-Cre mice.

165 rents activates muscarinic receptors on both vasoactive intestinal peptide-expressing (VIP) and parva

166 The relative weight of vasoactive intestinal peptide-expressing (Vip) interneur

167 In addition, vasoactive intestinal peptide-expressing axonal plexuses

168 Recent studies on vasoactive intestinal peptide-expressing inhibitory neur

169 Vasoactive intestinal peptide-expressing interneurons (V

170 Finally, vasoactive intestinal peptide-expressing interneurons pr

171 Optogenetic inhibition of vasoactive intestinal peptide-expressing neurons did not

172 ed controls is correlated with the number of vasoactive intestinal peptide-expressing SCN neurons.

173 More input to vasoactive intestinal peptide-positive (VIP+) neurons th

174 n-positive, somatostatin-positive (SST+), or vasoactive intestinal peptide-positive (VIP+) neurons, t

175 uted preferentially to surround suppression, vasoactive intestinal peptide-positive interneurons were

176 s primarily signaled motor action (licking), vasoactive intestinal peptide-positive neurons responded

177 id delivery and other issues associated with vasoactive intestinal peptide.

178 de-2, gastric-inhibitory peptide, and prepro-vasoactive intestinal peptide.

179 MP-generating agonists such as forskolin and vasoactive intestinal peptide.

180 ts parvalbumin (PV), somatostatin (SOM), and vasoactive intestinal peptitde (VIP)-expressing interneu

181 We demonstrate that interneurons expressing vasoactive intestinal polypeptide (VIP(+)) play a causal

182 Here, we show that interneurons expressing vasoactive intestinal polypeptide (VIP(+)) regulate the

183 hat type 3 IS (IS3) cells that coexpress the vasoactive intestinal polypeptide (VIP) and calretinin c

184 -dependent coupling process mediated by both vasoactive intestinal polypeptide (VIP) and GABAA signal

185 The neuropeptide vasoactive intestinal polypeptide (VIP) and its VPAC2 re

186 olar infusion of the VPAC1/2 receptor ligand vasoactive intestinal polypeptide (VIP) had no effect on

187 d determine the role of mast cells (MCs) and vasoactive intestinal polypeptide (VIP) in barrier regul

188 and alpha5-knockout mice, lower activity of vasoactive intestinal polypeptide (VIP) interneurons res

189 In mammals, vasoactive intestinal polypeptide (VIP) is known to have

190 Vasoactive intestinal polypeptide (VIP) is released from

191 ow that a class of interneurons that express vasoactive intestinal polypeptide (VIP) mediates disinhi

192 upled via gamma-aminobutyric acid (GABA) and vasoactive intestinal polypeptide (VIP) neurotransmitter

193 ssion and odor detection performance require vasoactive intestinal polypeptide (VIP) or its receptor

194 There is evidence that vasoactive intestinal polypeptide (VIP) participates in

195 Both secretin and vasoactive intestinal polypeptide (VIP) receptors are re

196 Vasoactive intestinal polypeptide (VIP) signaling is cri

197 ne hydroxylase, nitric oxide synthetase, and vasoactive intestinal polypeptide (VIP) to detect neural

198 Strikingly, vasoactive intestinal polypeptide (VIP), a neuropeptide

199 Paradoxically, we found that vasoactive intestinal polypeptide (VIP), a neuropeptide

200 rneurons expressing neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP), and the numeric

201 presence and colocalization of the peptides vasoactive intestinal polypeptide (VIP), calcitonin-gene

202 r GnIH inhibits the action of kisspeptin and vasoactive intestinal polypeptide (VIP), positive regula

203 circuit in frontal cortex that originates in vasoactive intestinal polypeptide (VIP)-expressing inter

204 , but not that of somatostatin-expressing or vasoactive intestinal polypeptide (VIP)-expressing inter

205 stance P (SP)-IR varicosities and 9 +/- 1.3% vasoactive intestinal polypeptide (VIP)-IR varicosities

206 ent manner by dorsal AH neurons that produce vasoactive intestinal polypeptide (VIP).

207 the structurally similar mammalian peptide, vasoactive intestinal polypeptide (VIP).

208 N, physiological evidence suggests that only vasoactive intestinal polypeptide (VIP)/gastrin-releasin

209 signaling pathways induced by kisspeptin and vasoactive intestinal polypeptide in GnRH neuronal cell

210 Although locomotion-induced vasoactive intestinal polypeptide positive (VIP) interne

211 oxylase, neuronal nitric oxide synthase, and vasoactive intestinal polypeptide to visualize neural el

212 s of somatostatin(+) (SST) (MGE-derived) and vasoactive intestinal polypeptide(+) (VIP) (CGE-derived)

213 s variant gene 1, substance P, somatostatin, vasoactive intestinal polypeptide, and parvalbumin.

214 co-localize with either cholecystokinin- or vasoactive intestinal polypeptide, but does with vasopre

215 for the specification of neuropeptide Y and vasoactive intestinal polypeptide, indicating that a sub

216 ndin, calretinin, parvalbumin, somatostatin, vasoactive intestinal polypeptide, neuropeptide Y, or ch

217 Immunoreactivity for vasoactive intestinal polypeptide, nitric oxide synthase

218 function, including cholinergic, adrenergic, vasoactive intestinal polypeptide, purinergic, androgen,

219 (MT), corticotropin-releasing hormone (CRH), vasoactive intestinal polypeptide, tyrosine hydroxylase,

220 pressing cyclooxygenase-2 (22%, p < 0.05) or vasoactive intestinal polypeptide-containing interneuron

221 re, we used a transgenic mouse line in which vasoactive intestinal polypeptide-expressing (VIP+) GABA

222 at in contrast to somatostatin-expressing or vasoactive intestinal polypeptide-expressing interneuron

223 tory neurons reduced their activity, whereas vasoactive intestinal polypeptide-expressing interneuron

224 inergic, adrenergic, and nitrergic axons and vasoactive intestinal polypeptide-positive terminals, so

225 injured unmyelinated afferents labeled with vasoactive intestinal polypeptide.

226 dal cells and GABA interneurons coexpressing vasoactive intestinal polypeptide.

227 Vasoactive liabilities are typically assayed using wire

228 ple cytochrome P450 eicosanoids, is a potent vasoactive lipid whose vascular effects include stimulat

229 scular permeability caused by the release of vasoactive mediator(s).

230 ics in vascular endothelium are modulated by vasoactive mediators and are critically involved in the

231 nse involving the rapid release of prestored vasoactive mediators followed by de novo synthesized pro

232 We conclude that therapies modulating vasoactive mediators or inflammatory cytokines may not a

233 of mast cells, leading to massive release of vasoactive mediators that induce acute hypotension and s

234 replication and the release of cytokines and vasoactive mediators, culminating in shock.

235 degranulation with release and secretion of vasoactive mediators, enzymes, and cytokines.

236 g mechanical ventilation (acute lung injury, vasoactive medication administration, delirium, renal re

237 ssure <90 mm Hg or the need for inotropic or vasoactive medication and the requirement for mechanical

238 ic drugs (odds ratio, 1.9; p = 0.03), higher vasoactive medication dose (odds ratio, 3.2; p = 0.02),

239 a, therapeutic intervention profiles such as vasoactive medication drip rates and ventilator settings

240 confidence interval, 2.7-24.9; P<0.01), and vasoactive medications (odds ratio, 5.7; 95% confidence

241 mpt administration of intravenous fluids and vasoactive medications aimed at restoring adequate circu

242 oxygenation, ventricular assist device, and vasoactive medications are independently associated with

243 Tailoring vasoactive medicines to patients with HF based upon bett

244 The CBF and CBV OTs suggest that vasoactive messengers are synthesized, released, and eff

245 efined functional gene group (thrombophilic, vasoactive, metabolic, immune, and cell signalling).

246 Importantly, the release of this vasoactive molecule must be both rapid and well controll

247 rm the blood-brain barrier (BBB) and release vasoactive molecules that regulate vascular tone.

248 in the splanchnic vascular bed, with several vasoactive molecules, controlled at multiple levels, wor

249 ility to cleave angiotensin I (Ang I) to the vasoactive octapeptide angiotensin II (Ang II), but is a

250 uscitation, fluid resuscitation > 5 L/24 hr, vasoactive or inotropic support, and renal replacement t

251 PVAT is a vasoactive organ with functional characteristics similar

252 s concluded that the pressor effect due to a vasoactive oxygen carrier may be beneficial in maintaini

253 FXR expression and involved intrahepatic vasoactive pathways (e.g., endothelial nitric oxide synt

254 We report the identification of the vasoactive peptide apelin as a central regulator for end

255 Serelaxin, recombinant human relaxin-2, is a vasoactive peptide hormone with many biological and haem

256 Angiotensin-II is a vasoactive peptide implicated in vascular physiology as

257 Adrenomedullin (ADM) is a circulating vasoactive peptide involved in vascular homeostasis and

258 drial ATP synthase F0 subunit component is a vasoactive peptide on its release from cells.

259 Endothelin-1 (ET-1) is a 21-amino acid vasoactive peptide that plays a key role in the pathogen

260 tected against barrier dysfunction caused by vasoactive peptide thrombin and proinflammatory bacteria

261 ds to overproduction of bradykinin, a potent vasoactive peptide.

262 Several endogenous vasoactive peptides act as adaptive mechanisms, and thei

263 ast, potentiation of endogenous compensatory vasoactive peptides can act to enhance the survival effe

264 , the two pathways are activated to generate vasoactive peptides that contribute in various ways to t

265 protective mechanisms mediated by estrogens, vasoactive peptides, and other hormones.

266 Endothelins are a family of vasoactive peptides, of which 3 distinct isoforms exist,

267 the capacity for production of hormones and vasoactive peptides.

268 n of the natriuretic peptides and many other vasoactive peptides.

269 -dependent production of prostanoids, mainly vasoactive PGE(2), and suggest that the coordinated down

270 Comparison of the relative vasoactive potencies and sympatholytic properties of ATP

271 that this elevates systemic levels of their vasoactive products, including chymase, and promotes vas

272 This study characterises the vasoactive properties of VEGF in isolated perfused pig r

273 noids that, among other actions, have strong vasoactive properties.

274 carbon monoxide-, or cytochrome p450-derived vasoactive prostanoid signaling but is associated with v

275 Elevated serum concentrations of the vasoactive protein endothelin-1 (ET-1) occur in the sett

276 Aqueous vasoactive protein levels were measured by protein array

277 Thirty-two vasoactive proteins were detected in aqueous in untreate

278 Aqueous levels of 55 vasoactive proteins were measured with protein array.

279 correlation between changes in levels of 13 vasoactive proteins with changes in EFT, including 3 kno

280 ynapses evokes the production and release of vasoactive signals from both neurons and astrocytes, whi

281 sponse to activation of endothelial cells by vasoactive signals such as endothelins.

282 the task of transmitting voltages induced by vasoactive signals, radial transmission is most efficien

283 ries is regulated by mechanical stresses and vasoactive signals.

284 tic, but rather, is dynamically modulated by vasoactive signals.

285 reactivity, the response of the vessels to a vasoactive stimulus such as hypoxia and hyperoxia, can b

286 ssible by the ability of RBCs to release the vasoactive substance adenosine triphosphate (ATP) in res

287 astrocytic activation, stimulates release of vasoactive substances and dilation of cerebral vasculatu

288 estration allowing for passage of diffusible vasoactive substances and interface of endothelial cell

289 It has been proposed that release of vasoactive substances by astrocytes couples neuronal act

290 of autophagy in the paracrine regulation of vasoactive substances from the endothelium.

291 (K(ATP)) channel is targeted by a variety of vasoactive substances, playing an important role in vasc

292 lude that while astrocytes can still release vasoactive substances, vascular amyloid deposits render

293 pulmonary hemorrhage, hypotension requiring vasoactive support, conduit disruption requiring covered

294 hemodynamics, and the activity of endogenous vasoactive systems (AEVS) were measured prospectively in

295 st hoc analysis of ROSE AHF, the response to vasoactive therapies differed in patients with heart fai

296 lysis may enable better individualization of vasoactive therapies in chronic HF and reduced ejection

297 Concomitant vasoactive therapy (odds ratio = 1.633; p < 0.001), medi

298 >/= 60 mm Hg, using normal saline bolus and vasoactive therapy-dopamine, and if needed noradrenaline

299 There was no interaction between vasoactive treatment's effect and EF on change in cystat

300 en when assessing the effect of inotrope and vasoactive treatments at 24, 48, and 72 hours.