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1                                              DOCA-salt hypertensive rats exhibited increased urinary
2                                              DOCA-salt myocytes demonstrated impaired relaxation, tau
3                                              DOCA-salt treatment resulted in significant elevation in
4                                              DOCA-salt treatment significantly increased renal tubula
5 g with ranolazine (DOCA-salt, 0.18 +/- 0.02, DOCA-salt+ranolazine, 0.13 +/- 0.01, sham, 0.11 +/- 0.01
6 31.9 +/- 2.8, sham+ranolazine, 30.2 +/- 1.9, DOCA-salt, 41.8 +/- 2.6, and DOCA-salt+ranolazine, 31.9
7 from the SFO to the OVLT and MnPO, abolishes DOCA-salt hypertension in the rat.
8 ts treated with deoxycorticosterone acetate (DOCA) and high salt.
9 sive (SHR), and deoxycorticosterone acetate (DOCA) hypertensive single cells of rat kidney interlobar
10 AC) surgery and deoxycorticosterone acetate (DOCA) pellet implantation.
11 er (L-NAME) and Deoxycorticosterone Acetate (DOCA) rat models.
12 plantation of a deoxycorticosterone acetate (DOCA) tablet (1% saline to drink) using rats on a low sa
13   Arteries from deoxycorticosterone acetate (DOCA)-salt and N(omega)-nitro-L-arginine (L-NNA) hyperte
14 jury induced by deoxycorticosterone acetate (DOCA)-salt compared to the controls.
15                 Deoxycorticosterone acetate (DOCA)-salt hypertension is characterized by a suppressed
16     We utilized deoxycorticosterone acetate (DOCA)-salt hypertension model in wild-type (WT) and B1R
17 lin-1 (ET-1) in deoxycorticosterone acetate (DOCA)-salt hypertension, a model of low renin hypertensi
18 so increased in deoxycorticosterone acetate (DOCA)-salt hypertension, which is associated with a mark
19 n the kidney in deoxycorticosterone acetate (DOCA)-salt hypertension.
20 re subjected to deoxycorticosterone acetate (DOCA)-salt hypertension; however, the duration of these
21          In the deoxycorticosterone acetate (DOCA)-salt model of hypertension, salt consumption contr
22 hypertension in deoxycorticosterone acetate (DOCA)-salt rats, a renin-independent model of hypertensi
23 otensin II- and deoxycorticosterone acetate (DOCA)-salt-induced hypertension.
24 sterone-mimetic deoxycorticosterone acetate (DOCA).
25 ole of CXCR6 in deoxycorticosterone acetate (DOCA)/salt-induced inflammation and fibrosis of the kidn
26 neralocorticoid deoxycorticosterone-acetate (DOCA) in combination with high salt intake induced arter
27 II infusion or desoxycorticosterone acetate (DOCA)-salt.
28 lemetrically 4 days before and 36 days after DOCA implantation (100 mg/rat; s.c.); 24-h sodium and wa
29 dysfunction, proteinuria, and fibrosis after DOCA-salt treatment compared with wild-type mice.
30  macrophages and T cells in the kidney after DOCA/salt treatment.
31 , 30.2 +/- 1.9, DOCA-salt, 41.8 +/- 2.6, and DOCA-salt+ranolazine, 31.9 +/- 2.6; P=0.018).
32 espectively, in LSD and even more in HSD and DOCA when entering dermis.
33 s ~2 and 4-5 times that of dermis in HSD and DOCA-salt.
34 hypertensive responses to angiotensin II and DOCA-salt challenge.
35 ing establishment of both Ang II-induced and DOCA salt hypertension, whereas a similar dose of nontar
36 hen given tap water to drink ad libitum, and DOCA-treated rats received a 0.9% NaCl solution to drink
37 nd p110delta density in aorta from L-NNA and DOCA-salt rats.
38 roxide in both ET-1-treated normotensive and DOCA-salt rats was reversed by a selective ET(A) recepto
39 2+)-activated CI- (CI(Ca)) currents, SHR and DOCA hypertensive Ca(2+)-activated K+ (K(Ca)) currents w
40 lular free [Ca2+] was greater in the SHR and DOCA hypertensive cells compared with control cells.
41        In current-clamp experiments, SHR and DOCA hypertensive cells were approximately 20 mV more de
42 o inhibit K(Ca) and CI(Ca) currents, SHR and DOCA hypertensive K(v) current was significantly smaller
43 ut mice were subjected to uninephrectomy and DOCA-salt treatment for 3 weeks.
44 angiotensin II; rats with uninephrectomy and DOCA-salt, or pulmonary artery banding; cardiomyocytes e
45 rols provided with normal drinking water and DOCA provided with DOCA pellets and sodium chloride drin
46  cardiac weight, and renal damage induced by DOCA-salt.
47 revented blood pressure elevation induced by DOCA-salt.
48  randomly divided into five groups: control, DOCA-salt, treated DOCA-salt-BFM, treated DOCA-salt-buty
49 t both were preserved in Tg-GCH mice despite DOCA-salt treatment.
50 xycorticosterone acetate and high-salt diet (DOCA-salt).
51                                    Following DOCA implantation, the magnitude of the elevation of MAP
52 ibroblast formation in the kidneys following DOCA-salt treatment.
53 -fold higher activity in thoracic aorta from DOCA-salt [systolic blood pressure (SBP)=184+/-5 mm Hg]
54 re expressed but not different in aorta from DOCA-salt and sham rats.
55  Ca2+-induced spontaneous tone in aorta from DOCA-salt rats.
56 tion to KCl and norepinephrine in aorta from DOCA-salt rats.
57       Detergent extracted fiber bundles from DOCA-salt hearts demonstrated increased myofilament resp
58  was significantly lower in homogenates from DOCA-salt rats.
59                                 Furthermore, DOCA treatment led to decreased expression of the slit d
60                                 Furthermore, DOCA-salt- treatment increased plasma arginine vasopress
61                                           In DOCA-salt rats, a very large increase in the intensity o
62  rings and reduced NADPH oxidase activity in DOCA-salt animals.
63 n prevented cardiac and renal dysfunction in DOCA-salt rats.
64 re-volume relationship slope was elevated in DOCA-salt mice, improving to sham levels with treatment
65  both the cortex and medulla were greater in DOCA-salt rats compared with placebo-treated animals.
66  puncta counts were significantly greater in DOCA-salt rats than controls.
67 prevented the development of hypertension in DOCA-salt rats and reduced blood pressure of SHRs to nor
68 elium-dependent relaxations were impaired in DOCA-salt rats, conditions that were improved by apocyni
69 ersus 72+/-3%, P<0.05) were also impaired in DOCA-salt.
70 teric arteries was significantly improved in DOCA-salt-treated Tg-GCH mice, in parallel with reduced
71 w endothelin-1 (ET-1), which is increased in DOCA-salt hypertensive rats, contributes to arterial sup
72 ide (NK3r agonist) attenuates salt intake in DOCA-treated animals.
73 re we examined whether CXCL16 is involved in DOCA-salt-induced renal inflammation and fibrosis.
74 decreased GTPCH I activity and BH4 levels in DOCA-salt compared with sham rats.
75  for the increased renal production of NO in DOCA-salt hypertension, and are consistent with a role f
76 ared with sham controls but was preserved in DOCA-salt-treated Tg-GCH mice.
77 itant decrease of systolic blood pressure in DOCA-salt rats.
78 ling; all of these effects were prevented in DOCA-salt-treated Tg-GCH mice.
79 r endothelium-dependent vessel relaxation in DOCA-salt rats, excluding a role of a local renin/angiot
80 dependent relaxation and basal NO release in DOCA-salt rats.
81 ation and lipid accumulation were studied in DOCA-salt treated rats.
82 nd deoxycorticosterone acetate-salt-induced (DOCA-salt-induced) cardiovascular organ damage and hyper
83                                  In WT mice, DOCA-salt-treatment increased gene and protein expressio
84 ce were further subjected to the nephrectomy/DOCA (deoxycorticosterone acetate) model of diastolic dy
85 0beta protein density, but neither L-NNA nor DOCA-salt had differences in p85alpha and p110alpha.
86 ignificantly elevated in carotid arteries of DOCA-salt rats compared with that of the sham-operated c
87                     Treatment of arteries of DOCA-salt rats with the selective ETA receptor antagonis
88 sed superoxide levels in carotid arteries of DOCA-salt rats.
89 dothelial dysfunction in carotid arteries of DOCA-salt rats.
90 eated them with a range of concentrations of DOCA and found a dose-dependent decrease in NK3r-mRNA ab
91 n (SFO); are required for the development of DOCA-salt hypertension.
92 al convoluted tubule (DCT) in the kidneys of DOCA-salt mice and CD8(+) T cell-injected mice, leading
93                                 Treatment of DOCA-salt rats with serelaxin decreased renal inflammati
94                            During 3 weeks of DOCA-salt treatment, arterial blood pressure was increas
95 ia, and kidney fibrosis after three weeks of DOCA/salt treatment.
96 e uninephrectomized, and either a placebo or DOCA pellet was implanted subcutaneously.
97  relaxation, tau, improving with ranolazine (DOCA-salt, 0.18 +/- 0.02, DOCA-salt+ranolazine, 0.13 +/-
98               In summary, serelaxin reversed DOCA-salt induced cardiac and renal dysfunction.
99  mice with deoxycorticosterone acetate-salt (DOCA-salt) hypertension, ROS production from NO synthase
100 t diet and deoxycorticosterone acetate-salt (DOCA-salt) treatments, but BP control remained intact.
101 receptors are downregulated after subchronic DOCA treatment and this finding is consistent with the h
102                                          TAC/DOCA cRbm20(DeltaRRM)-DMSO mice developed LV hypertrophy
103   LV chamber stiffness was normalized in TAC/DOCA cRbm20(DeltaRRM)-raloxifene mice that expressed N2B
104 ant improvement in exercise tolerance in TAC/DOCA mice that expressed N2BAsc.
105  was equally increased in both groups of TAC/DOCA mice (cRbm20(DeltaRRM)-DMSO and cRbm20(DeltaRRM)-ra
106 c function and exercise tolerance in the TAC/DOCA model.
107 in a renovascular model of hypertension, the DOCA-salt rat, and if these changes are preventable by n
108                      Oxidative stress in the DOCA-salt model may increase late I(Na), resulting in di
109 required for hypertension development in the DOCA-salt model.
110 iminishes self-directed saline intake in the DOCA-salt rat.
111                           After 4 weeks, the DOCA-salt rats were randomly selected and implanted with
112 blunts the increase in blood pressure due to DOCA-salt hypertension.
113 ecovery of PGC-1alpha expression response to DOCA-salt challenge in offspring that underwent prenatal
114 infiltration into the kidneys in response to DOCA-salt hypertension.
115 minuria and glomerular damage in response to DOCA.
116 dividual contribution of these structures to DOCA-salt hypertension is unknown.
117 enylephrine was delayed in mice subjected to DOCA-salt or chronic delivery of angiotensin II.
118 BFM, treated DOCA-salt-butyrate, and treated DOCA-salt-acetate, for 5 weeks.
119 l, DOCA-salt, treated DOCA-salt-BFM, treated DOCA-salt-butyrate, and treated DOCA-salt-acetate, for 5
120 nto five groups: control, DOCA-salt, treated DOCA-salt-BFM, treated DOCA-salt-butyrate, and treated D
121 io, was decreased significantly in wild-type DOCA-salt mice compared with sham controls but was prese
122 ly 100-microm outside diameter) in wild-type DOCA-salt mice exists, evidenced by increased medial cro
123 ls were decreased significantly in wild-type DOCA-salt mice, but both were preserved in Tg-GCH mice d
124 versus sham+ranolazine, 0.18 +/- 0.01 versus DOCA-salt, 0.23 +/- 0.2 versus DOCA-salt+ranolazine, 0.1
125 - 0.01 versus DOCA-salt, 0.23 +/- 0.2 versus DOCA-salt+ranolazine, 0.17 +/- 0.0 1 mm Hg/L; P<0.005).
126                           To examine whether DOCA's effects on NK3r synthesis are direct, we used dif
127 ly minimally altered in vessels of mice with DOCA-salt hypertension but seems to be mediated by hydro
128 normal drinking water and DOCA provided with DOCA pellets and sodium chloride drinking water.
129                  Thus, we injected rats with DOCA once daily for 11 days and analyzed tachykinin rece
130                       Rats were treated with DOCA and saline drinking water for 3 weeks.
131 ression of hypertension in mice treated with DOCA-salt.
132 pe and CXCR6 knockout mice were treated with DOCA/salt for 3 weeks.
133 ut mice at baseline and after treatment with DOCA/salt.
134 and kidney fibrosis following treatment with DOCA/salt.
135 lasts in the kidney following treatment with DOCA/salt.

 
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