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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.
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
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
49 ), we demonstrated that, on enhanced cardiac renin-angiotensin system activity, Cav1 dissociated from
51 en cholesterol, brain glucose, and the brain renin-angiotensin system, all of which are affected in s
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
61 ate-induced hypertensive effect involves the renin-angiotensin system and is abolished in GPR91-defic
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
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,
78 ne >/=160 mumol/l; hemoglobin </=120 g/l; no renin-angiotensin system antagonist; and no beta-blocker
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
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
91 hieve statistical significance in benefit of renin-angiotensin system blockade on their primary combi
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
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
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
113 al Agt gene expression and activation of the renin-angiotensin system, by which hyperglycemia induces
116 modulated in part by local activation of the renin-angiotensin system, compound the hyperglycemia-ind
120 rease in the vasoprotective axis of the lung renin-angiotensin system, decreased inflammatory cytokin
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
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
138 nical benefits produced by inhibitors of the renin-angiotensin system in heart failure has been modes
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
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
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-
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
157 tested, including maximal inhibition of the renin-angiotensin system, inhibition of renal intracellu
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
168 These observations demonstrate that the renin-angiotensin system is a key mediator of lung fibro
170 ting evidence has suggested that the cardiac renin-angiotensin system is activated during the remodel
172 tudies demonstrating that suppression of the renin-angiotensin system is associated with muted vascul
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
178 ed renin is pivotal for activating a cardiac renin-angiotensin system leading to excessive norepineph
180 ndicate that pharmacological blockade of the renin-angiotensin system may be considered for primary A
182 tensin II (AngII), the major effector of the renin-angiotensin system, mediates kidney disease progre
184 t that ACE2 is a functional component of the renin-angiotensin system, metabolizing Ang II and thereb
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
190 homeostatically responding component of the renin-angiotensin system, one of the most important regu
193 Alzheimer's disease pathophysiology and the renin angiotensin system pathways suggest that angiotens
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
202 se, therapies that inhibit components of the renin angiotensin system (RAS) are also indicated, but t
214 e of antihypertensive peptides acting on the renin-angiotensin system (RAS) and the endothelin (ET) s
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
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
225 ), which reduces albuminuria, in addition to renin-angiotensin system (RAS) blockade, can slow progre
229 s suggest that activation of the circulating renin-angiotensin system (RAS) develops in aP2-HSD1 mice
233 tics than nondiabetics and activation of the renin-angiotensin system (RAS) has been implicated, the
237 essure, reflecting the important role of the renin-angiotensin system (RAS) in controlling body fluid
248 paB activation, endothelium dysfunction, and renin-angiotensin system (RAS) over-activity in thoracic
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
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
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
278 , which do not counteract any longer the CPC renin-angiotensin system, resulting in cellular senescen
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
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
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
294 nds upon stimulation of AS expression by the renin-angiotensin system, which takes 12 h to reach full
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
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