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1 +) intake regardless of the presence of high deoxycorticosterone acetate.
2 cement therapy with either corticosterone or deoxycorticosterone acetate.
3 studied 2 weeks later) mice without and with deoxycorticosterone acetate administration, all in the s
4 ension driven by combined uninephrectomy and deoxycorticosterone acetate administration.
5 sfunction mouse models were studied: (1) TAC-deoxycorticosterone acetate and (2) Lepr(db/db).
6                                    Exogenous deoxycorticosterone acetate and deletion of the P2Y(2) r
7 vels in thoracic aortas when challenged with deoxycorticosterone acetate and high-salt diet (DOCA-sal
8 er the induction of severe hypertension with deoxycorticosterone acetate and salt, proteinuria, impai
9 ed left ventricular chamber stiffness in TAC-deoxycorticosterone acetate, but not in Lepr(db/db) mice
10 ust sodium appetite (e.g., sodium depletion, deoxycorticosterone acetate) decrease lateral hypothalam
11 ase-3 (NOS3) expression in rats treated with deoxycorticosterone acetate (DOCA) and high salt.
12  (SD), spontaneously hypertensive (SHR), and deoxycorticosterone acetate (DOCA) hypertensive single c
13 sverse aortic constriction (TAC) surgery and deoxycorticosterone acetate (DOCA) pellet implantation.
14 )-Nitro-L-arginine Methyl Ester (L-NAME) and Deoxycorticosterone Acetate (DOCA) rat models.
15  1% saline to drink) or by implantation of a deoxycorticosterone acetate (DOCA) tablet (1% saline to
16                                Arteries from deoxycorticosterone acetate (DOCA)-salt and N(omega)-nit
17 ertensive mice with kidney injury induced by deoxycorticosterone acetate (DOCA)-salt compared to the
18                                              Deoxycorticosterone acetate (DOCA)-salt hypertension is
19                                  We utilized deoxycorticosterone acetate (DOCA)-salt hypertension mod
20 ugmented by increased endothelin-1 (ET-1) in deoxycorticosterone acetate (DOCA)-salt hypertension, a
21 scular superoxide level is also increased in deoxycorticosterone acetate (DOCA)-salt hypertension, wh
22 ound that CXCL16 is induced in the kidney in deoxycorticosterone acetate (DOCA)-salt hypertension.
23  ChR2-expressing mice that were subjected to deoxycorticosterone acetate (DOCA)-salt hypertension; ho
24                                       In the deoxycorticosterone acetate (DOCA)-salt model of hyperte
25 CT7263 (BFM) would attenuate hypertension in deoxycorticosterone acetate (DOCA)-salt rats, a renin-in
26 th CTLA4-Ig reduced both angiotensin II- and deoxycorticosterone acetate (DOCA)-salt-induced hyperten
27 hat are administered the aldosterone-mimetic deoxycorticosterone acetate (DOCA).
28  study, we investigated the role of CXCR6 in deoxycorticosterone acetate (DOCA)/salt-induced inflamma
29      Administration of the mineralocorticoid deoxycorticosterone-acetate (DOCA) in combination with h
30 ropriate for salt status, mineralocorticoid (deoxycorticosterone acetate) excess causes hypertrophy,
31           Compared with sham mice, sham plus deoxycorticosterone acetate mice had mild hypertrophy wi
32 on mice, transverse aortic constriction plus deoxycorticosterone acetate mice had similar left ventri
33 lar matrix proteins in LVs of uninephrectomy/deoxycorticosterone acetate mice, which correlated with
34  relaxation was unimpaired in uninephrectomy/deoxycorticosterone acetate mice.
35 d in intact cardiomyocytes isolated from TAC-deoxycorticosterone acetate mice.
36 rs left ventricular chamber stiffness in TAC-deoxycorticosterone acetate mice.
37 e further subjected to the nephrectomy/DOCA (deoxycorticosterone acetate) model of diastolic dysfunct
38  prevented decreases in the ECu50 induced by deoxycorticosterone acetate-no salt treatment.
39 taneous implantation of a controlled-release deoxycorticosterone acetate pellet, and given 1% saline
40 s after uninephrectomy and implantation with deoxycorticosterone acetate pellets, when DD was clearly
41  inflammatory pathways in the development of deoxycorticosterone acetate salt hypertension.
42 ed CKD, unilateral ureteric obstruction, and deoxycorticosterone acetate salt unilateral nephrectomy
43 d inflammasome activation in mouse models of deoxycorticosterone acetate salt-induced hypertension as
44 ion per se were studied in uninephrectomized deoxycorticosterone acetate salt-treated rats, where the
45                       In aortas of mice with deoxycorticosterone acetate-salt (DOCA-salt) hypertensio
46 se in RMR in response to a high-fat diet and deoxycorticosterone acetate-salt (DOCA-salt) treatments,
47 pes in the brain, ADAM17 upregulation during deoxycorticosterone acetate-salt hypertension occurs sel
48 y and attenuates Ang II (angiotensin II) and deoxycorticosterone acetate-salt induced hypertension.
49         To test this hypothesis, we used the deoxycorticosterone acetate-salt model of neurogenic hyp
50 ebrospinal fluid of nontransgenic mice after deoxycorticosterone acetate-salt treatment and were acco
51                                              Deoxycorticosterone acetate-salt treatment in nontransge
52 have shown that stimuli like angiotensin II, deoxycorticosterone acetate-salt, and excessive catechol
53 tory factor, in angiotensin II- (ANGII-) and deoxycorticosterone acetate-salt-induced (DOCA-salt-indu
54  sodium channel inhibitor, in a rat model of deoxycorticosterone acetate, unilateral nephrectomy, and