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1 lance between the classic and vasoprotective renin angiotensin system.
2 malized by pharmacological inhibition of the renin-angiotensin system.
3 N-gamma-induced activation of the intrarenal renin-angiotensin system.
4 zyme-2 (ACE2) is a negative regulator of the renin-angiotensin system.
5 It is hypothesized to be a new member of the renin-angiotensin system.
6 y uncharacterized feedback loop in the local renin-angiotensin system.
7 he pro(renin) receptor and activation of the renin-angiotensin system.
8 ovel understanding of pathophysiology of the renin-angiotensin system.
9 l injury at least in part by suppressing the renin-angiotensin system.
10 early administration of drugs that block the renin-angiotensin system.
11 lete and thus more effective blockade of the renin-angiotensin system.
12  to have opposing physiological roles to the renin-angiotensin system.
13 ed pharmacologic approach to blockade of the renin-angiotensin system.
14 e renin-1d enzyme in a local juxtaglomerular renin-angiotensin system.
15 e genotyped for 32 SNPs on five genes in the renin-angiotensin system.
16 s required for the adrenergic control of the renin-angiotensin system.
17 d by weight reduction and/or blockade of the renin-angiotensin system.
18 omain is sufficient to maintain a functional renin-angiotensin system.
19  of renin and constitute a unique extrarenal renin-angiotensin system.
20 t also, in part, via activation of the local renin-angiotensin system.
21 enzyme inhibitors (ACEI) to downregulate the renin-angiotensin system.
22 the haplotype structure in four genes of the renin-angiotensin system.
23 eart diseases associated with an upregulated renin-angiotensin system.
24  a novel negative endocrine regulator of the renin-angiotensin system.
25 (V-ATPase) that may also function within the renin-angiotensin system.
26 ne or in combination with antagonists of the renin-angiotensin system.
27 ortant for regulating blood pressure via the renin-angiotensin system.
28  including inflammation, thrombosis, and the renin-angiotensin system.
29 ay be caused by a dysregulation of the local renin/angiotensin system.
30 eduction via the plasma kallikrein/kinin and renin angiotensin systems.
31 ulated through both the central and systemic renin-angiotensin systems.
32 ence of numerous independent tissue-specific renin-angiotensin systems.
33               In addition to the traditional renin-angiotensin system, a great deal of evidence favor
34  rate-limiting step in the activation of the renin-angiotensin system, a key modulator of body fluid
35 howed that a mouse model (ACE8/8) of cardiac renin-angiotensin system activation has a high rate of s
36                                              Renin-angiotensin system activation is a feature of many
37                                              Renin-angiotensin system activation is associated with a
38                                              Renin-angiotensin system activation is associated with c
39             Hypertension caused by increased renin-angiotensin system activation is associated with e
40 ffects that are preserved in the presence of renin-angiotensin system activation or heart failure.
41 n-13 infusions in the presence or absence of renin-angiotensin system activation with sodium depletio
42 for an overlapping role of oxidative stress, renin-angiotensin system activation, and dyslipidemia in
43 rtant reactive oxygen species sources during renin-angiotensin system activation, with different Nox
44 e effective antiarrhythmic drugs in cases of renin-angiotensin system activation.
45 ing prolonged (Pyr(1))apelin-13 infusion and renin-angiotensin system activation.
46  in disease states characterized by enhanced renin-angiotensin system activation.
47 rotect against tissue injury associated with renin-angiotensin system activation.
48 mic risk in cardiac diseases associated with renin-angiotensin system activation.
49 ), we demonstrated that, on enhanced cardiac renin-angiotensin system activity, Cav1 dissociated from
50 henotypes that may indirectly reflect tissue renin-angiotensin system activity.
51 en cholesterol, brain glucose, and the brain renin-angiotensin system, all of which are affected in s
52                          In recent years the renin-angiotensin system, already of recognised importan
53 lso studied the consequential effects on the renin angiotensin system and blood pressure.
54 that vitamin D deficiency activates both the renin angiotensin system and macrophage ER stress to con
55 further assess the interaction between brain renin-angiotensin system and ADAM17, we generated mice l
56              RGS5 signaling is linked to the renin-angiotensin system and directly controls vascular
57                     A cross-talk between the renin-angiotensin system and EGFR signaling was elicited
58                                          The renin-angiotensin system and especially the angiotensin
59                       Insulin stimulates the renin-angiotensin system and induces renal vasodilation.
60        Collectrin is an orphan member of the renin-angiotensin system and is a homolog of angiotensin
61 ate-induced hypertensive effect involves the renin-angiotensin system and is abolished in GPR91-defic
62           Because VDR ablation activates the renin-angiotensin system and leads to accumulation of an
63           ACE2 may play a unique role in the renin-angiotensin system and mediate cardiovascular and
64  inhibitors with drugs that inhibit both the renin-angiotensin system and neprilysin.
65 t activation and fibrosis in response to the renin-angiotensin system and post-MI remodeling.
66 failure is associated with activation of the renin-angiotensin system and skeletal muscle wasting.
67 e to classic signaling pathways, such as the renin-angiotensin system and sympathetic nervous system.
68  further evidence implicating the intrarenal renin-angiotensin system and take us one step further by
69 hereby suggesting that targeting of both the renin-angiotensin system and the EP1 receptor could be b
70     Renin is the rate-limiting enzyme in the renin-angiotensin system and thus dictates the level of
71 expression of the hAGT, up-regulation of the renin angiotensin system, and increased blood pressure a
72 landins serve as important modulators of the renin-angiotensin system, and cross-talk exists between
73  diabetes associated with stimulation of the renin-angiotensin system, and further studies to assess
74 salt and fluid reabsorption, antagonizes the renin-angiotensin system, and inhibits oxidative stress.
75 and the mechanism involves activation of the renin-angiotensin system; and (iv) podocytes undergo typ
76 between the two key enzymes of the pulmonary renin-angiotensin system, angiotensin-converting enzyme,
77                       Agents that target the renin-angiotensin system--angiotensin-converting enzyme
78 ne >/=160 mumol/l; hemoglobin </=120 g/l; no renin-angiotensin system antagonist; and no beta-blocker
79             Patients received beta-blockers, renin-angiotensin system antagonists, and statins withou
80 olesterolemia greatly augmented the systemic renin-angiotensin system, as demonstrated by large incre
81 ce the survival effects of inhibitors of the renin-angiotensin system, as evidenced by trials that ha
82 e of dual inhibitors that interfere with the renin-angiotensin system at multiple sites have not yiel
83      Stopping the detrimental effects of the renin-angiotensin system at the most upstream point of t
84 ngiotensin system that regulates the classic renin angiotensin system axis.
85 inning this hypertension is an overactivated renin angiotensin system because ACE inhibition reverses
86 s not the result of enhanced activity of the renin-angiotensin system because circulating renin conce
87 edication, and a greater proportion received renin angiotensin system blockade (RASB) compared with i
88 dition of aliskiren to standard therapy with renin-angiotensin system blockade in patients with type
89 tion suggest a possible therapeutic role for renin-angiotensin system blockade in reducing heart fail
90                Available data on the role of renin-angiotensin system blockade in renal transplantati
91 hieve statistical significance in benefit of renin-angiotensin system blockade on their primary combi
92                                              Renin-angiotensin system blockade therapy is associated
93 progressed to ESRD, the other seven received renin-angiotensin system blockade, and one also received
94 iduals with autosomal recessive disease with renin-angiotensin system blockade, possibly even before
95 rtive care alone, mostly involving optimized renin-angiotensin system blockade, which might generate
96 complimentary pharmacology and more complete renin-angiotensin system blockade.
97 ffect is amplified when BP is controlled via renin-angiotensin system blockade.
98 perglycaemic drugs, insulin, or both, plus a renin-angiotensin system blocker and an additional antih
99  with diabetes and hypertension, combining a renin-angiotensin system blocker with amlodipine, compar
100 on) trial compared the outcomes effects of a renin-angiotensin system blocker, benazepril, combined w
101 I, 0.72-0.76]; P < .001), and those who used renin-angiotensin system blockers (OR, 0.24 [95% CI, 0.0
102     Results of previous studies suggest that renin-angiotensin system blockers might reduce the burde
103 ntihypertensive therapy that did not include renin-angiotensin system blockers was administered to ac
104 associations between treatment with statins, renin-angiotensin system blockers, beta-blockers, dual a
105 l stiffness, such as exercise and the use of renin-angiotensin system blockers, may be protective aga
106 3-6 months of optimized supportive care with renin-angiotensin system blockers.
107 pertensive regimens without beta-blockers or renin-angiotensin system blocking agents.
108 ed by hyperinsulinemia and activation of the renin-angiotensin system, both of which are associated w
109 ific deletion of Atp6ap2 does not affect the renin-angiotensin system but causes a combination of ren
110 tance and attenuated local expression of the renin-angiotensin system but did not prevent adverse LV
111                            Inhibition of the renin-angiotensin system by amniotic fluid stem cells ma
112 ing enzyme inhibitors and ARBs interrupt the renin-angiotensin system by distinct mechanisms.
113 al Agt gene expression and activation of the renin-angiotensin system, by which hyperglycemia induces
114                            The expression of renin-angiotensin system components was determined at 15
115  cardiovascular function by regulating other renin-angiotensin system components.
116 modulated in part by local activation of the renin-angiotensin system, compound the hyperglycemia-ind
117                                 Although the renin-angiotensin system contributes to fibrogenesis and
118                    It is well known that the renin-angiotensin system contributes to left ventricular
119                                 Although the renin-angiotensin system contributes to the progression
120 rease in the vasoprotective axis of the lung renin-angiotensin system, decreased inflammatory cytokin
121 n prescribing (lipid-lowering, antiplatelet, renin-angiotensin system drugs).
122          Pharmacological interruption of the renin-angiotensin system focuses on optimization of bloc
123 ng AngII, working in tandem with the central renin-angiotensin system, further exacerbates sympatho-h
124 n, a combination of genotype variants of the renin-angiotensin system genes is a powerful determinant
125         New evidence suggests that the brain renin angiotensin system has two opposing pathways: a da
126                            Inhibition of the renin-angiotensin system has been suggested to decrease
127                         In recent years, the renin-angiotensin system has emerged as a key mediator o
128 n deleterious aspects of "stress." While the renin-angiotensin system has received some attention in
129 Newer drugs, including agents that block the renin-angiotensin system, have improved the level of BP
130 egies to target this important member of the renin-angiotensin system holds potential for the develop
131 f vitamin D receptor (VDR) and activation of renin angiotensin system; however, the involved mechanis
132  might help explain the relation between the renin-angiotensin system, hypertension, and Alzheimer's
133     Loss of ACE2 disrupts the balance of the renin-angiotensin system in a diabetic state and leads t
134 absorption through reciprocal effects on the renin-angiotensin system in a way that facilitates salt
135 icle further confirms the involvement of the renin-angiotensin system in cardiac fibrosis and illustr
136                 Activation of the endogenous renin-angiotensin system in Cyp1a1Ren2 transgenic rats r
137 ation of renin release and activation of the renin-angiotensin system in health and disease.
138 nical benefits produced by inhibitors of the renin-angiotensin system in heart failure has been modes
139 (NSE-AT(1a)) to unmask the role of the brain renin-angiotensin system in hypertension.
140                        Early blockade of the renin-angiotensin system in patients with type 1 diabete
141              The recognition of the role the renin-angiotensin system in promoting insulin resistance
142                                Modifying the renin-angiotensin system in sepsis should be further eva
143 e in vivo effects of CNIs on the local renal renin-angiotensin system in the collecting duct (CD).
144 hm in both tissues and downregulation of the renin-angiotensin system in the kidney and mitogen-activ
145                     Although the role of the renin-angiotensin system in the pathophysiology of hyper
146 ta suggest that glucose can activate a local renin-angiotensin system in the podocyte, leading to inc
147  provides evidence supporting a role for the renin-angiotensin system in the regulation of the stress
148 opment of hypertension, thus implicating the renin-angiotensin system in this process.
149                 Activation of the endogenous renin-angiotensin system in transgenic Cyp1a1Ren2 rats r
150 e evidence of involvement of nociception and renin-angiotensin systems in this effect.
151 30 mmHg, in conjunction with blockade of the renin-angiotensin system, in patients with type 2 diabet
152  increase in c-Src activity may help mediate renin-angiotensin system-induced arrhythmias and that c-
153                                              Renin-angiotensin system-induced Cav1 S-nitrosation was
154 n albuminuria, similar to that observed with renin-angiotensin system inhibition (losartan plus enala
155  provide complementary beneficial effects to renin-angiotensin system inhibition to slow progression
156  target of the vascular protective action of renin-angiotensin system inhibition.
157  tested, including maximal inhibition of the renin-angiotensin system, inhibition of renal intracellu
158 IEW: Angioedema is a serious complication of renin-angiotensin system inhibitor therapy.
159  with diabetic nephropathy on chronic stable renin-angiotensin system inhibitor treatment.
160                 Calcium channel blockers and renin-angiotensin system inhibitors are associated with
161                 Thus, TGF-beta1 mAb added to renin-angiotensin system inhibitors did not slow progres
162 tation could help to broaden the benefits of renin-angiotensin system inhibitors for patients with he
163 for targeting mast cells in conjunction with renin-angiotensin system inhibitors in the management of
164 mostly but not entirely under treatment with renin-angiotensin system inhibitors.
165 ive cellular environment without confounding renin-angiotensin system interactions.
166            Pharmacological inhibition of the renin-angiotensin system is a common approach to treat h
167                                          The renin-angiotensin system is a coordinated hormonal casca
168      These observations demonstrate that the renin-angiotensin system is a key mediator of lung fibro
169                    Overactivity of the brain renin-angiotensin system is a major contributor to neuro
170 ting evidence has suggested that the cardiac renin-angiotensin system is activated during the remodel
171                                  Because the renin-angiotensin system is activated in many catabolic
172 tudies demonstrating that suppression of the renin-angiotensin system is associated with muted vascul
173                    Dysregulation of the skin renin-angiotensin system is implicated in abnormal wound
174                              Blockade of the renin-angiotensin system is renoprotective in a variety
175 in-kinin system, along with the interlocking renin-angiotensin system, is a key regulator of vascular
176  (ACE), one of the central components of the renin-angiotensin system, is a key therapeutic target fo
177                     After stimulation of the renin-angiotensin system, juxtaglomerular cells containe
178 ed renin is pivotal for activating a cardiac renin-angiotensin system leading to excessive norepineph
179                              Blockade of the renin-angiotensin system lowers UAER, but whether this e
180 ndicate that pharmacological blockade of the renin-angiotensin system may be considered for primary A
181           Long-term alterations of the brain renin-angiotensin system may influence signaling pathway
182 tensin II (AngII), the major effector of the renin-angiotensin system, mediates kidney disease progre
183                        We measured levels of renin-angiotensin system messenger RNA and proteins in s
184 t that ACE2 is a functional component of the renin-angiotensin system, metabolizing Ang II and thereb
185            Insulin-induced activation of the renin-angiotensin system modulates insulin-induced renal
186 gies in terms of dosing and effectiveness of renin-angiotensin system-modulating agents for treatment
187 nt a unique paradigm for understanding local renin-angiotensin systems, not just in the heart, but in
188     As most of the biological effects of the renin-angiotensin system occur through stimulation of th
189             Treatment with inhibitors of the renin-angiotensin system often decreases the rate of pro
190  homeostatically responding component of the renin-angiotensin system, one of the most important regu
191           Experimental studies implicate the renin-angiotensin system, particularly angiotensin II ty
192                     Recently, an alternative renin-angiotensin system pathway has been described, whi
193  Alzheimer's disease pathophysiology and the renin angiotensin system pathways suggest that angiotens
194                    Chronic activation of the renin-angiotensin system plays a deleterious role in pro
195           There is growing evidence that the renin-angiotensin system plays a key role in the pathoge
196                                          The renin-angiotensin system plays an important role in card
197                                          The renin-angiotensin system plays an important role in the
198 or (HGF) gene therapy with inhibition of the renin-angiotensin system produced synergistic beneficial
199  host factors, such as the activation of the renin-angiotensin system, promote the progression of occ
200 ngiotensin II, the principal effector of the renin-angiotensin system, promotes vasoconstriction by a
201                            Although both the renin angiotensin system (RAS) and the paired homeobox 2
202 se, therapies that inhibit components of the renin angiotensin system (RAS) are also indicated, but t
203              Most physiologic effects of the renin angiotensin system (RAS) are mediated via the angi
204                                          The renin angiotensin system (RAS) has been implicated as on
205                        The activation of the renin angiotensin system (RAS) has been implicated in th
206                                Recently, the renin angiotensin system (RAS) has been shown to regulat
207                              The role of the renin angiotensin system (RAS) in atherosclerosis is com
208              Inappropriate activation of the renin angiotensin system (RAS) is a key contributor to t
209                                              Renin angiotensin system (RAS) is a key hormonal system
210                 Activation of the intrarenal renin angiotensin system (RAS) is believed to play an im
211                        While blockade of the renin angiotensin system (RAS) is beneficial in treating
212                                          The renin-angiotensin system (RAS) and angiotensin AT1 recep
213                                          The renin-angiotensin system (RAS) and reactive oxygen speci
214 e of antihypertensive peptides acting on the renin-angiotensin system (RAS) and the endothelin (ET) s
215            Based on the critical role of the renin-angiotensin system (RAS) and the type I (AT1) angi
216 significance of cross-regulation between the renin-angiotensin system (RAS) and tumor necrosis factor
217 ought association of genetic variants in the renin-angiotensin system (RAS) and vitamin D system with
218 ac outpatient clinic for the up-titration of renin-angiotensin system (RAS) antagonists and beta-bloc
219                      A functioning placental renin-angiotensin system (RAS) appears necessary for unc
220                            Components of the renin-angiotensin system (RAS) are expressed in a number
221 Physicians have embraced the concept of dual renin-angiotensin system (RAS) blockade hoping that it w
222  clinical studies have shown the benefits of renin-angiotensin system (RAS) blockade in the developme
223                                              Renin-angiotensin system (RAS) blockade reduces mortalit
224            Data are lacking on the effect of renin-angiotensin system (RAS) blockade therapy with ang
225 ), which reduces albuminuria, in addition to renin-angiotensin system (RAS) blockade, can slow progre
226 and persistent proteinuria despite optimised renin-angiotensin system (RAS) blockade.
227                 Activation of the intrarenal renin-angiotensin system (RAS) can elicit hypertension i
228              Inappropriate activation of the renin-angiotensin system (RAS) contributes to many CKDs.
229 s suggest that activation of the circulating renin-angiotensin system (RAS) develops in aP2-HSD1 mice
230                     Furthermore, ACE and the renin-angiotensin system (RAS) directly regulate hemangi
231              Inappropriate activation of the renin-angiotensin system (RAS) exacerbates renal and vas
232                                   An altered renin-angiotensin system (RAS) has been implicated as a
233 tics than nondiabetics and activation of the renin-angiotensin system (RAS) has been implicated, the
234                                          The renin-angiotensin system (RAS) has emerged as a key path
235          Medications aimed at inhibiting the renin-angiotensin system (RAS) have been used extensivel
236         The increased activity of intrarenal renin-angiotensin system (RAS) in a setting of elevated
237 essure, reflecting the important role of the renin-angiotensin system (RAS) in controlling body fluid
238 ephropathy already receiving stable doses of renin-angiotensin system (RAS) inhibitors.
239                                          The renin-angiotensin system (RAS) is a key regulator of the
240                                          The renin-angiotensin system (RAS) is a principal determinan
241                                          The renin-angiotensin system (RAS) is activated in heart fai
242                                          The renin-angiotensin system (RAS) is an important regulator
243               Pathological activation of the renin-angiotensin system (RAS) is associated with the me
244                   The circulating, endocrine renin-angiotensin system (RAS) is important to circulato
245                            Activation of the renin-angiotensin system (RAS) may contribute to the dev
246                                          The renin-angiotensin system (RAS) mediates proapoptotic, pr
247                                              Renin-angiotensin system (RAS) modulator therapy is indi
248 paB activation, endothelium dysfunction, and renin-angiotensin system (RAS) over-activity in thoracic
249                          The products of the renin-angiotensin system (RAS) play an important role in
250                                          The renin-angiotensin system (RAS) plays a critical role in
251                                          The renin-angiotensin system (RAS) plays a major role in liv
252           Recent evidence indicates that the renin-angiotensin system (RAS) plays a major role in liv
253                                          The renin-angiotensin system (RAS) plays an important role i
254                   It has been shown that the renin-angiotensin system (RAS) plays key roles in the de
255                                          The renin-angiotensin system (RAS) plays pathogenic roles in
256                                          The renin-angiotensin system (RAS) regulates blood pressure
257                                          The renin-angiotensin system (RAS) regulates BP and may affe
258  renewed interest in therapies targeting the renin-angiotensin system (RAS) to improve beta-cell func
259 mpus is associated with gene variants of the renin-angiotensin system (RAS), a system implicated in v
260 zyme 2 (ACE2) is a negative regulator of the renin-angiotensin system (RAS), catalyzing the conversio
261 iac mast cells (MC), thus activating a local renin-angiotensin system (RAS), culminating in ventricul
262                    Here, we propose that the renin-angiotensin system (RAS), in addition to its centr
263  At comparable BP control, inhibitors of the renin-angiotensin system (RAS), including angiotensin co
264 ced glomerular filtration, activation of the renin-angiotensin system (RAS), oxidative/nitrative stre
265 onic kidney disease and up-regulation of the renin-angiotensin system (RAS), which is deleterious to
266 diabetes mellitus includes activation of the renin-angiotensin system (RAS), which may lead to hypert
267  evidence for a regulatory role in the human renin-angiotensin system (RAS).
268 on from cardiac mast cells activates a local renin-angiotensin system (RAS).
269 center for the cardiovascular actions of the renin-angiotensin system (RAS).
270 chanism for blood pressure regulation by the renin-angiotensin system (RAS).
271 elated with the RPF response to blocking the renin-angiotensin system (RAS).
272       While both the endothelin-1 (ET-1) and renin-angiotensin systems (RAS) are activated in congest
273  are frequently associated with an activated renin-angiotensin-system (RAS) and increased levels of i
274 bitors or angiotensin receptor blockers (ie, renin-angiotensin system [RAS] antagonists) did not reac
275  and provide evidence that inhibition of the renin-angiotensin system reduces glomerulosclerosis in a
276           Notably, 10-week inhibition of the renin-angiotensin system regenerated kidney vasculature
277                            Activation of the renin angiotensin system resulting in stimulation of ang
278 , which do not counteract any longer the CPC renin-angiotensin system, resulting in cellular senescen
279                   Despite suppression of the renin-angiotensin system, salt loading enhances oxidativ
280                                TGF-beta1 and renin-angiotensin system signaling alters the fibroblast
281 Antihypertensive medications that target the renin angiotensin system, such as angiotensin receptor b
282  factor-like ligand 1A and components of the renin-angiotensin system, support the importance of IL-1
283                           beta1-RB decreases renin-angiotensin system sympathostimulation and activat
284 ary enzyme of the vasoprotective axis of the renin angiotensin system that regulates the classic reni
285 dogenous 7-amino acid peptide hormone of the renin-angiotensin system that has antiproliferative prop
286 that activation of the protective arm of the renin angiotensin system, the angiotensin-converting enz
287 hypertensive agents that did not inhibit the renin-angiotensin system to reach targets of under 135 m
288           The contribution of the intrarenal renin-angiotensin system to the development of hypertens
289 sults demonstrate the existence of an airway renin-angiotensin system triggered by release of mast-ce
290 portive care (in particular, blockade of the renin-angiotensin system) was adjusted on the basis of p
291 ssociated with an imbalance of the pulmonary renin-angiotensin system, which correlates with aggravat
292        LS diet induces the activation of the renin-angiotensin system, which increases oxidative stre
293              Inappropriate activation of the renin-angiotensin system, which plays a central role in
294 nds upon stimulation of AS expression by the renin-angiotensin system, which takes 12 h to reach full
295                              Blockade of the renin-angiotensin system with angiotensin-converting enz
296 sted the hypothesis that interruption of the renin-angiotensin system with either an angiotensin-conv
297      These studies are the first to link the renin-angiotensin system with the fibrinolytic system to
298  [Ang-(1-7)] is an endogenous peptide of the renin-angiotensin system with vasodilator and antiprolif
299                  Much is known about a local renin-angiotensin system within the uteroplacental vascu
300                               In the central renin-angiotensin system, zinc-dependent aminopeptidase

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