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1 duced when focusing on drugs that affect the renin angiotensin-aldosterone system.
2 tubular injury and aberrant upregulation of renin-angiotensin aldosterone system.
3 nefits in association with inhibition of the renin-angiotensin-aldosterone system.
4 ation of both the circulating and intrarenal renin-angiotensin-aldosterone system.
5 es are in part a result of activation of the renin-angiotensin-aldosterone system.
6 be related to circulating biomarkers of the renin-angiotensin-aldosterone system.
7 oxygen in the renal cortex and activates the renin-angiotensin-aldosterone system.
8 pathogenic variants in genes involved in the Renin-Angiotensin-Aldosterone System.
9 suria and natriuresis without changes in the Renin-Angiotensin-Aldosterone System.
10 pregnant women partly through the suppressed renin-angiotensin-aldosterone system.
11 ome, and the roles of the nervous system and renin-angiotensin-aldosterone system.
12 ood pressure control through blockade of the renin-angiotensin-aldosterone system.
13 important, yet controversial, members of the renin-angiotensin-aldosterone system.
14 absorption despite reduced activation of the renin-angiotensin-aldosterone system.
15 AT1R and AT2R serve as key components of the renin-angiotensin-aldosterone system.
16 ted to racial differences in activity of the renin-angiotensin-aldosterone system.
17 , 20 mmol/d) diet to activate the endogenous renin-angiotensin-aldosterone system.
18 , and the use of medications that affect the renin-angiotensin-aldosterone system.
19 t processes conventionally attributed to the renin-angiotensin-aldosterone system.
20 stemic blood pressure, and inhibition of the renin-angiotensin-aldosterone system.
21 either stimulation or nonstimulation of the renin/angiotensin/aldosterone system.
22 inogen is the most upstream precursor of the renin-angiotensin-aldosterone system, a key pathway in b
23 ivity, endothelial and vasodilator function, renin angiotensin aldosterone system activation), and th
26 rn of positive associations of biomarkers of renin-angiotensin-aldosterone system activation with pan
30 ular endothelial cells and by regulating the renin-angiotensin-aldosterone system, adiposity, energy
31 activation (B-type natriuretic peptide), and renin-angiotensin-aldosterone system (aldosterone and re
33 drug treatment (including inhibitors of the renin-angiotensin-aldosterone system and beta blockers)
34 n therapy, excluding other inhibitors of the renin-angiotensin-aldosterone system and beta-blockers.
35 ion of solute and water by hormones from the renin-angiotensin-aldosterone system and by antidiuretic
37 n and oxidative stress, maladaptation of the renin-angiotensin-aldosterone system and coagulation sys
38 chanisms of heart failure: activation of the renin-angiotensin-aldosterone system and decreased sensi
39 y pregnancy is coupled to stimulation of the renin-angiotensin-aldosterone system and hypotonicity.
40 a paradigm shift in our understanding of the renin-angiotensin-aldosterone system and in aldosterone'
41 lar macrophages as additional players in the renin-angiotensin-aldosterone system and introduce a nov
42 re advanced heart failure, activation of the renin-angiotensin-aldosterone system and is related to w
43 he purpose of this review is to describe the renin-angiotensin-aldosterone system and its regulatory
46 es a brief update on the organization of the renin-angiotensin-aldosterone system and other angiotens
47 at this is mediated by interactions with the renin-angiotensin-aldosterone system and reactive oxygen
48 pressure syndromes predominantly involve the renin-angiotensin-aldosterone system and the adrenal glu
49 ilure (HF) is based on interference with the renin-angiotensin-aldosterone system and the adrenergic
51 nd around the kidneys, (2) activation of the renin-angiotensin-aldosterone system, and (3) increased
52 ion of adverse remodeling, inhibition of the renin-angiotensin-aldosterone system, and favorable meta
53 cose transporter with a possible role in the renin-angiotensin-aldosterone system, and hypertension (
54 evels of parathyroid hormone, activating the renin-angiotensin-aldosterone system, and increasing ins
55 lasma and urine biochemistry, markers of the renin-angiotensin-aldosterone system, and oxidative stre
56 eased total kidney volume, activation of the renin-angiotensin-aldosterone system, and progression of
57 iuretic peptides and proteins related to the renin-angiotensin-aldosterone system; and (4) metabolism
59 enrollment size; North American; that tested renin-angiotensin-aldosterone system antagonists and ant
60 hort study on patients with DMD treated with renin-angiotensin-aldosterone system antagonists with or
63 confirmed that certain lipoproteins and the renin-angiotensin-aldosterone system are important in th
64 ming growth factor-beta1 (TGF-beta1) and the renin-angiotensin-aldosterone system are key mediators i
66 y heart period rhythms are influenced by the renin-angiotensin-aldosterone system, as low and respira
67 95% CI, 1.61-1.83; P<.001) and received more renin-angiotensin-aldosterone system-based therapy at fo
69 mization strategies, steroid minimization or renin-angiotensin-aldosterone system blockade result in
70 such as blood pressure and glucose control, renin-angiotensin-aldosterone system blockade, statin th
72 ong 52 studies selected in first phase, only renin-angiotensin-aldosterone-system blockade vs. placeb
74 patients (27.5%) had either beta blocker or renin-angiotensin-aldosterone system blocker administere
75 alence and outcomes associated with beta and renin-angiotensin-aldosterone system blocker therapy in
77 igher-than-usual antihypertensive dosages of renin-angiotensin-aldosterone system blockers may provid
78 was higher in patients who received beta or renin-angiotensin-aldosterone system blockers prior to c
80 Compared with patients not given beta or renin-angiotensin-aldosterone system blockers, the 30-da
81 of glomerulonephritis, which despite use of renin-angiotensin-aldosterone-system blockers and immuno
82 ns is influenced by genetic variation in the renin-angiotensin-aldosterone system, but no clinical tr
84 This shows that increased activity of the renin-angiotensin-aldosterone system contributes to incr
86 ation of renin or significant interaction of renin-angiotensin-aldosterone system drugs with renin in
87 r understand it effects on the dysfunctional renin-angiotensin-aldosterone system during vasoplegic s
88 the cellular effects of sex hormones on the renin-angiotensin-aldosterone system, endothelial respon
89 described, suggesting the possibility that a renin-angiotensin-aldosterone system exists in the heart
93 mperfectly understood, although an activated renin-angiotensin aldosterone system has been implicated
96 ensin-converting enzyme 2 depletion disrupts renin-angiotensin-aldosterone system homeostasis, favori
97 ated during the entire 6-h protocol, whereas renin-angiotensin-aldosterone system hormones were withi
100 r of these flux pathways is regulated by the renin-angiotensin-aldosterone system; however, the mecha
101 y Syndrome Coronavirus-2) has implicated the renin-angiotensin-aldosterone system in acute respirator
102 ar filtration rate without activation of the renin-angiotensin-aldosterone system in experimental CHF
103 he importance of different components of the renin-angiotensin-aldosterone system in heart failure bu
104 ls have helped to add insight on the role of renin-angiotensin-aldosterone system in heart failure.
105 trophy, consistent with a major role for the renin-angiotensin-aldosterone system in LV remodeling.
106 risk related to medications that act on the renin-angiotensin-aldosterone system in patients exposed
108 As are combined with other inhibitors of the renin-angiotensin-aldosterone system in patients with HF
109 is under negative-feedback regulation by the renin-angiotensin-aldosterone system in protection of so
110 t, under salt restriction, activation of the renin-angiotensin-aldosterone system in the kidney compe
111 in combination with other inhibitors of the renin-angiotensin-aldosterone system increases the risk
112 retic, glomerular filtration rate enhancing, renin-angiotensin-aldosterone system inhibiting, cardiac
113 achieving remission than patients receiving renin-angiotensin-aldosterone system inhibition alone.
115 ascular events on top of maximally tolerated renin-angiotensin-aldosterone system inhibition in patie
117 prone to reverse-causation bias as stopping renin angiotensin aldosterone system inhibitor therapy i
119 ability to enable specified target doses of renin-angiotensin-aldosterone system inhibitor (RAASi) u
120 kalemia is a common complication of taking a renin-angiotensin-aldosterone system inhibitor (RAASi).
121 terone system inhibitor group versus the non-renin-angiotensin-aldosterone system inhibitor group (10
122 inhibitor group versus 69.7 mm Hg in the non-renin-angiotensin-aldosterone system inhibitor group (p
123 al pressure at 6 hours was 72.2 mm Hg in the renin-angiotensin-aldosterone system inhibitor group ver
124 were significantly lower at 24 hours in the renin-angiotensin-aldosterone system inhibitor group ver
126 r requirements at 24 hours compared with non-renin-angiotensin-aldosterone system inhibitor patients.
127 two cohorts: 1) patients who were on chronic renin-angiotensin-aldosterone system inhibitor therapy a
128 ents and 2) patients who were not on chronic renin-angiotensin-aldosterone system inhibitor therapy a
129 ts receiving vasopressin who were on chronic renin-angiotensin-aldosterone system inhibitor therapy v
130 ts receiving vasopressin who were on chronic renin-angiotensin-aldosterone system inhibitor therapy w
131 eceiving vasopressin who were not on chronic renin-angiotensin-aldosterone system inhibitor therapy.
132 chronic obstructive pulmonary disease, BMI, renin-angiotensin-aldosterone system inhibitor use, and
133 were receiving beta-blockers, 71% received a renin-angiotensin-aldosterone system inhibitor, 29% rece
134 elets, beta-blockers, and statins as well as renin-angiotensin-aldosterone system inhibitors (OR, 0.8
135 ociation between depression and adherence to renin-angiotensin-aldosterone system inhibitors (OR, 0.9
136 y statins (OR, 1.10; 95% CI, 1.00-1.21), and renin-angiotensin-aldosterone system inhibitors (OR, 1.2
137 nverting enzyme 2 (ACE2), but whether or not renin-angiotensin-aldosterone system inhibitors (RAASi)
138 telets 87% to 96%; beta-blockers 69% to 85%; renin-angiotensin-aldosterone system inhibitors 46% to 7
139 of beta-blockers, n = 20; and withdrawal of renin-angiotensin-aldosterone system inhibitors and beta
142 n, subjects were randomized to withdrawal of renin-angiotensin-aldosterone system inhibitors and/or b
144 ns the risk of hyperkalemia, especially when renin-angiotensin-aldosterone system inhibitors are used
146 , we use 50,821 patient records to find that renin-angiotensin-aldosterone system inhibitors have a p
147 outcomes in infected individuals and whether renin-angiotensin-aldosterone system inhibitors have det
148 yperkalemia, as well as the potential use of renin-angiotensin-aldosterone system inhibitors in patie
149 78.0%) in NHANES 2005-2008 (P <.001); use of renin-angiotensin-aldosterone system inhibitors increase
150 reater; before and for 2 days after surgery, renin-angiotensin-aldosterone system inhibitors were wit
151 reater; before and for 2 days after surgery, renin-angiotensin-aldosterone system inhibitors were wit
152 (antiplatelets, beta-blockers, statins, and renin-angiotensin-aldosterone system inhibitors) initiat
153 clinical trials have established the role of renin-angiotensin-aldosterone system inhibitors, beta bl
154 hormonal activation in patients treated with renin-angiotensin-aldosterone system inhibitors, its pot
155 moral blocker therapy, n = 20; withdrawal of renin-angiotensin-aldosterone system inhibitors, n = 20;
156 rest: non-steroidal anti-inflammatory drugs, renin-angiotensin-aldosterone system inhibitors, or prot
157 atients on target doses of beta-blockers and renin-angiotensin-aldosterone system inhibitors, respect
159 rent DKD treatments have expanded to include renin-angiotensin-aldosterone system inhibitors, sodium-
160 whom new and existing cardiorenal therapies (renin-angiotensin-aldosterone system inhibitors, sodium-
164 e treated with nonspecific therapies such as renin-angiotensin-aldosterone system inhibitors; however
166 cardioprotective medications (betablockers, renin-angiotensin-aldosterone-system inhibitors, statins
167 n four clinical trials testing the effect of renin-angiotensin-aldosterone system intervention on alb
169 uggesting that a cardioprotective arm of the renin-angiotensin-aldosterone system is active in HF.
173 on in Tetralogy of Fallot: Inhibition of the Renin-Angiotensin-Aldosterone System) is an investigator
174 ood but probably involve disturbances of the renin-angiotensin-aldosterone system, loss of endogenous
177 Renal function and circulating levels of renin-angiotensin-aldosterone system mediators and NO we
178 th expressed in the kidney and implicated in renin-angiotensin-aldosterone system modulated immune re
179 by aldosterone, a critical component of the Renin-Angiotensin-Aldosterone-System, modulates inflamma
180 review the recent developments pertaining to renin-angiotensin-aldosterone system modulation therapy
181 a complex neurohumoral system including the renin-angiotensin-aldosterone system, natriuretic peptid
182 such as beta-blockers and inhibitors of the renin-angiotensin-aldosterone system, newer agents have
183 tion between chronic sodium appetite and the renin-angiotensin-aldosterone system on LHSS reward.
184 ondrial signaling producing downstream RAAS (renin-angiotensin-aldosterone system) overactivation and
185 s homeostasis by measuring components of the renin-angiotensin-aldosterone system, parathyroid hormon
187 its the optimal use of agents that block the renin-angiotensin-aldosterone system, particularly in pa
188 e anti-fibrotic effects of inhibitors of the renin-angiotensin-aldosterone system, perhaps supplantin
191 ntricular hypertrophy, but inhibitors of the renin-angiotensin-aldosterone system possess the most po
193 lume homeostasis includes suppression of the renin-angiotensin-aldosterone system, pressure natriures
194 eptide of the counter-regulatory axis of the renin-angiotensin-aldosterone system previously demonstr
195 enzyme 2, and consequently, deregulates the renin-angiotensin-aldosterone system, promoting importan
199 6-day low-sodium diet was used to stimulate renin-angiotensin-aldosterone system (RAAS) activation,
200 fluid homeostasis through its action in the renin-angiotensin-aldosterone system (RAAS) and the rena
201 ompensate, neurohormonal systems such as the renin-angiotensin-aldosterone system (RAAS) and the symp
202 ter balance and cardiovascular function: the renin-angiotensin-aldosterone system (RAAS) and the symp
203 nsin-converting enzyme inhibitors (ACEi) for renin-angiotensin-aldosterone system (RAAS) blockade are
204 he effectiveness and safety of SGLT2i versus renin-angiotensin-aldosterone system (RAAS) blockade in
205 ad been raised about the potential effect of renin-angiotensin-aldosterone system (RAAS) blockades on
206 ht to investigate the influence of recipient renin-angiotensin-aldosterone system (RAAS) genotype on
207 eath and limits the use of inhibitors of the renin-angiotensin-aldosterone system (RAAS) in high-risk
208 rsening renal function (WRF) associated with renin-angiotensin-aldosterone system (RAAS) inhibition d
209 Although podocyte number is higher after renin-angiotensin-aldosterone system (RAAS) inhibition i
210 score of at least 1 and not already using a renin-angiotensin-aldosterone system (RAAS) inhibitor we
211 doses to treat patients with heart failure, renin-angiotensin-aldosterone system (RAAS) inhibitors i
212 predominantly seen in patients treated with renin-angiotensin-aldosterone system (RAAS) inhibitors w
213 g conditions such as hypertension and are on renin-angiotensin-aldosterone system (RAAS) inhibitors.
214 lacebo (both in addition to supportive care [renin-angiotensin-aldosterone system (RAAS) inhibitors]
220 in circulating ANP without activation of the renin-angiotensin-aldosterone system (RAAS) or sodium re
224 and release is the rate-limiting step of the renin-angiotensin-aldosterone system (RAAS) that control
225 drome coronavirus-2 that interfaces with the renin-angiotensin-aldosterone system (RAAS) through angi
226 (AGEs), oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and subclin
227 eptin replacement, but not inhibition of the renin-angiotensin-aldosterone system (RAAS), resulted in
230 stay of treatment for CKD is blockade of the renin-angiotensin-aldosterone system (RAAS), which reduc
243 and dogs with heart disease to mitigate the renin-angiotensin-aldosterone system (RAAS); however, th
244 of angiotensin II (assessment of intrarenal renin-angiotensin-aldosterone system [RAAS]) were measur
246 progression in db/db eNOS-/- mice receiving renin-angiotensin-aldosterone system (RAS)-blocking drug
247 dependent on a sustained suppression of the renin-angiotensin-aldosterone system rather than on natr
248 ptide), oxidative stress (homocysteine), the renin-angiotensin-aldosterone system (renin and aldoster
249 he natriuretic peptide and kinin systems and renin-angiotensin-aldosterone system, respectively.
250 f aldosterone is typically controlled by the renin-angiotensin-aldosterone system, situated in the ad
251 activation (with increased activation of the renin-angiotensin-aldosterone system, the sympathetic ne
252 AGT, suggesting an impaired response of the renin-angiotensin-aldosterone system to hypovolemic and
253 of sympathetic and vagal mechanisms and the renin-angiotensin-aldosterone system to very-low-frequen
254 en by various pathways that include hypoxia, renin-angiotensin-aldosterone system, transforming growt
256 c variables and use of drugs that act on the renin-angiotensin-aldosterone system were recorded prosp
257 out mice exhibited similar activation of the renin-angiotensin-aldosterone system, whereas only dKO m
258 m was to determine whether inhibitors of the renin-angiotensin-aldosterone system, which can reduce v
259 d systemic and intra-renal activation of the renin-angiotensin-aldosterone-system, which further limi
260 hypertension treatment via modulation of the renin-angiotensin-aldosterone system with angiotensin re
261 proteinuria have been based on blocking the renin-angiotensin-aldosterone system with the use of ang
262 e sympathetic activation via the upregulated renin-angiotensin-aldosterone system, without changing i
263 w explores convergent pathways involving the renin-angiotensin-aldosterone system, Wnt/beta-catenin s