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1 AT1R and AT2R serve as key components of the renin-angiotensin-aldosterone system.
2 be related to circulating biomarkers of the renin-angiotensin-aldosterone system.
3 , 20 mmol/d) diet to activate the endogenous renin-angiotensin-aldosterone system.
4 , and the use of medications that affect the renin-angiotensin-aldosterone system.
5 t processes conventionally attributed to the renin-angiotensin-aldosterone system.
6 stemic blood pressure, and inhibition of the renin-angiotensin-aldosterone system.
7 nefits in association with inhibition of the renin-angiotensin-aldosterone system.
8 ation of both the circulating and intrarenal renin-angiotensin-aldosterone system.
9 es are in part a result of activation of the renin-angiotensin-aldosterone system.
10 either stimulation or nonstimulation of the renin/angiotensin/aldosterone system.
12 rn of positive associations of biomarkers of renin-angiotensin-aldosterone system activation with pan
15 ular endothelial cells and by regulating the renin-angiotensin-aldosterone system, adiposity, energy
16 activation (B-type natriuretic peptide), and renin-angiotensin-aldosterone system (aldosterone and re
18 n therapy, excluding other inhibitors of the renin-angiotensin-aldosterone system and beta-blockers.
19 ion of solute and water by hormones from the renin-angiotensin-aldosterone system and by antidiuretic
21 chanisms of heart failure: activation of the renin-angiotensin-aldosterone system and decreased sensi
22 y pregnancy is coupled to stimulation of the renin-angiotensin-aldosterone system and hypotonicity.
23 a paradigm shift in our understanding of the renin-angiotensin-aldosterone system and in aldosterone'
24 he purpose of this review is to describe the renin-angiotensin-aldosterone system and its regulatory
27 es a brief update on the organization of the renin-angiotensin-aldosterone system and other angiotens
28 at this is mediated by interactions with the renin-angiotensin-aldosterone system and reactive oxygen
29 ilure (HF) is based on interference with the renin-angiotensin-aldosterone system and the adrenergic
30 nd around the kidneys, (2) activation of the renin-angiotensin-aldosterone system, and (3) increased
31 evels of parathyroid hormone, activating the renin-angiotensin-aldosterone system, and increasing ins
32 eased total kidney volume, activation of the renin-angiotensin-aldosterone system, and progression of
33 enrollment size; North American; that tested renin-angiotensin-aldosterone system antagonists and ant
34 hort study on patients with DMD treated with renin-angiotensin-aldosterone system antagonists with or
36 confirmed that certain lipoproteins and the renin-angiotensin-aldosterone system are important in th
37 ming growth factor-beta1 (TGF-beta1) and the renin-angiotensin-aldosterone system are key mediators i
38 y heart period rhythms are influenced by the renin-angiotensin-aldosterone system, as low and respira
39 95% CI, 1.61-1.83; P<.001) and received more renin-angiotensin-aldosterone system-based therapy at fo
41 mization strategies, steroid minimization or renin-angiotensin-aldosterone system blockade result in
43 ong 52 studies selected in first phase, only renin-angiotensin-aldosterone-system blockade vs. placeb
44 patients (27.5%) had either beta blocker or renin-angiotensin-aldosterone system blocker administere
45 alence and outcomes associated with beta and renin-angiotensin-aldosterone system blocker therapy in
47 igher-than-usual antihypertensive dosages of renin-angiotensin-aldosterone system blockers may provid
48 was higher in patients who received beta or renin-angiotensin-aldosterone system blockers prior to c
50 Compared with patients not given beta or renin-angiotensin-aldosterone system blockers, the 30-da
51 ns is influenced by genetic variation in the renin-angiotensin-aldosterone system, but no clinical tr
54 described, suggesting the possibility that a renin-angiotensin-aldosterone system exists in the heart
58 mperfectly understood, although an activated renin-angiotensin aldosterone system has been implicated
62 r of these flux pathways is regulated by the renin-angiotensin-aldosterone system; however, the mecha
63 ar filtration rate without activation of the renin-angiotensin-aldosterone system in experimental CHF
64 he importance of different components of the renin-angiotensin-aldosterone system in heart failure bu
65 ls have helped to add insight on the role of renin-angiotensin-aldosterone system in heart failure.
66 trophy, consistent with a major role for the renin-angiotensin-aldosterone system in LV remodeling.
68 As are combined with other inhibitors of the renin-angiotensin-aldosterone system in patients with HF
69 is under negative-feedback regulation by the renin-angiotensin-aldosterone system in protection of so
70 t, under salt restriction, activation of the renin-angiotensin-aldosterone system in the kidney compe
71 in combination with other inhibitors of the renin-angiotensin-aldosterone system increases the risk
72 retic, glomerular filtration rate enhancing, renin-angiotensin-aldosterone system inhibiting, cardiac
75 terone system inhibitor group versus the non-renin-angiotensin-aldosterone system inhibitor group (10
76 inhibitor group versus 69.7 mm Hg in the non-renin-angiotensin-aldosterone system inhibitor group (p
77 were significantly lower at 24 hours in the renin-angiotensin-aldosterone system inhibitor group ver
78 al pressure at 6 hours was 72.2 mm Hg in the renin-angiotensin-aldosterone system inhibitor group ver
80 r requirements at 24 hours compared with non-renin-angiotensin-aldosterone system inhibitor patients.
81 two cohorts: 1) patients who were on chronic renin-angiotensin-aldosterone system inhibitor therapy a
82 ents and 2) patients who were not on chronic renin-angiotensin-aldosterone system inhibitor therapy a
83 ts receiving vasopressin who were on chronic renin-angiotensin-aldosterone system inhibitor therapy v
84 ts receiving vasopressin who were on chronic renin-angiotensin-aldosterone system inhibitor therapy w
85 eceiving vasopressin who were not on chronic renin-angiotensin-aldosterone system inhibitor therapy.
86 telets 87% to 96%; beta-blockers 69% to 85%; renin-angiotensin-aldosterone system inhibitors 46% to 7
87 ns the risk of hyperkalemia, especially when renin-angiotensin-aldosterone system inhibitors are used
88 yperkalemia, as well as the potential use of renin-angiotensin-aldosterone system inhibitors in patie
89 78.0%) in NHANES 2005-2008 (P <.001); use of renin-angiotensin-aldosterone system inhibitors increase
92 n four clinical trials testing the effect of renin-angiotensin-aldosterone system intervention on alb
93 uggesting that a cardioprotective arm of the renin-angiotensin-aldosterone system is active in HF.
97 on in Tetralogy of Fallot: Inhibition of the Renin-Angiotensin-Aldosterone System) is an investigator
98 ood but probably involve disturbances of the renin-angiotensin-aldosterone system, loss of endogenous
100 Renal function and circulating levels of renin-angiotensin-aldosterone system mediators and NO we
101 review the recent developments pertaining to renin-angiotensin-aldosterone system modulation therapy
102 such as beta-blockers and inhibitors of the renin-angiotensin-aldosterone system, newer agents have
103 tion between chronic sodium appetite and the renin-angiotensin-aldosterone system on LHSS reward.
105 e anti-fibrotic effects of inhibitors of the renin-angiotensin-aldosterone system, perhaps supplantin
108 ntricular hypertrophy, but inhibitors of the renin-angiotensin-aldosterone system possess the most po
109 lume homeostasis includes suppression of the renin-angiotensin-aldosterone system, pressure natriures
110 eptide of the counter-regulatory axis of the renin-angiotensin-aldosterone system previously demonstr
112 fluid homeostasis through its action in the renin-angiotensin-aldosterone system (RAAS) and the rena
113 ompensate, neurohormonal systems such as the renin-angiotensin-aldosterone system (RAAS) and the symp
114 nsin-converting enzyme inhibitors (ACEi) for renin-angiotensin-aldosterone system (RAAS) blockade are
115 ht to investigate the influence of recipient renin-angiotensin-aldosterone system (RAAS) genotype on
116 eath and limits the use of inhibitors of the renin-angiotensin-aldosterone system (RAAS) in high-risk
117 rsening renal function (WRF) associated with renin-angiotensin-aldosterone system (RAAS) inhibition d
118 Although podocyte number is higher after renin-angiotensin-aldosterone system (RAAS) inhibition i
119 doses to treat patients with heart failure, renin-angiotensin-aldosterone system (RAAS) inhibitors i
120 predominantly seen in patients treated with renin-angiotensin-aldosterone system (RAAS) inhibitors w
125 in circulating ANP without activation of the renin-angiotensin-aldosterone system (RAAS) or sodium re
128 (AGEs), oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and subclin
129 eptin replacement, but not inhibition of the renin-angiotensin-aldosterone system (RAAS), resulted in
139 of angiotensin II (assessment of intrarenal renin-angiotensin-aldosterone system [RAAS]) were measur
141 dependent on a sustained suppression of the renin-angiotensin-aldosterone system rather than on natr
142 ptide), oxidative stress (homocysteine), the renin-angiotensin-aldosterone system (renin and aldoster
143 of sympathetic and vagal mechanisms and the renin-angiotensin-aldosterone system to very-low-frequen
145 out mice exhibited similar activation of the renin-angiotensin-aldosterone system, whereas only dKO m
146 m was to determine whether inhibitors of the renin-angiotensin-aldosterone system, which can reduce v
147 proteinuria have been based on blocking the renin-angiotensin-aldosterone system with the use of ang
148 e sympathetic activation via the upregulated renin-angiotensin-aldosterone system, without changing i
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