ライフサイエンスコーパス: DOCA

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 Arteries from deoxycorticosterone acetate (DOCA)-salt and N(omega)-nitro-L-arginine (L-NNA) hyperte

12 jury induced by deoxycorticosterone acetate (DOCA)-salt compared to the controls.

13 Deoxycorticosterone acetate (DOCA)-salt hypertension is characterized by a suppressed

14 lin-1 (ET-1) in deoxycorticosterone acetate (DOCA)-salt hypertension, a model of low renin hypertensi

15 so increased in deoxycorticosterone acetate (DOCA)-salt hypertension, which is associated with a mark

16 n the kidney in deoxycorticosterone acetate (DOCA)-salt hypertension.

17 otensin II- and deoxycorticosterone acetate (DOCA)-salt-induced hypertension.

18 sterone-mimetic deoxycorticosterone acetate (DOCA).

19 neralocorticoid deoxycorticosterone-acetate (DOCA) in combination with high salt intake induced arter

20 II infusion or desoxycorticosterone acetate (DOCA)-salt.

21 lemetrically 4 days before and 36 days after DOCA implantation (100 mg/rat; s.c.); 24-h sodium and wa

22 dysfunction, proteinuria, and fibrosis after DOCA-salt treatment compared with wild-type mice.

23 , 30.2 +/- 1.9, DOCA-salt, 41.8 +/- 2.6, and DOCA-salt+ranolazine, 31.9 +/- 2.6; P=0.018).

24 hypertensive responses to angiotensin II and DOCA-salt challenge.

25 ing establishment of both Ang II-induced and DOCA salt hypertension, whereas a similar dose of nontar

26 hen given tap water to drink ad libitum, and DOCA-treated rats received a 0.9% NaCl solution to drink

27 nd p110delta density in aorta from L-NNA and DOCA-salt rats.

28 roxide in both ET-1-treated normotensive and DOCA-salt rats was reversed by a selective ET(A) recepto

29 2+)-activated CI- (CI(Ca)) currents, SHR and DOCA hypertensive Ca(2+)-activated K+ (K(Ca)) currents w

30 lular free [Ca2+] was greater in the SHR and DOCA hypertensive cells compared with control cells.

31 In current-clamp experiments, SHR and DOCA hypertensive cells were approximately 20 mV more de

32 o inhibit K(Ca) and CI(Ca) currents, SHR and DOCA hypertensive K(v) current was significantly smaller

33 ut mice were subjected to uninephrectomy and DOCA-salt treatment for 3 weeks.

34 rols provided with normal drinking water and DOCA provided with DOCA pellets and sodium chloride drin

35 revented blood pressure elevation induced by DOCA-salt.

36 t both were preserved in Tg-GCH mice despite DOCA-salt treatment.

37 xycorticosterone acetate and high-salt diet (DOCA-salt).

38 Following DOCA implantation, the magnitude of the elevation of MAP

39 ibroblast formation in the kidneys following DOCA-salt treatment.

40 -fold higher activity in thoracic aorta from DOCA-salt [systolic blood pressure (SBP)=184+/-5 mm Hg]

41 re expressed but not different in aorta from DOCA-salt and sham rats.

42 Ca2+-induced spontaneous tone in aorta from DOCA-salt rats.

43 tion to KCl and norepinephrine in aorta from DOCA-salt rats.

44 Detergent extracted fiber bundles from DOCA-salt hearts demonstrated increased myofilament resp

45 was significantly lower in homogenates from DOCA-salt rats.

46 Furthermore, DOCA treatment led to decreased expression of the slit d

47 In DOCA-salt rats, a very large increase in the intensity o

48 n prevented cardiac and renal dysfunction in DOCA-salt rats.

49 re-volume relationship slope was elevated in DOCA-salt mice, improving to sham levels with treatment

50 both the cortex and medulla were greater in DOCA-salt rats compared with placebo-treated animals.

51 puncta counts were significantly greater in DOCA-salt rats than controls.

52 prevented the development of hypertension in DOCA-salt rats and reduced blood pressure of SHRs to nor

53 elium-dependent relaxations were impaired in DOCA-salt rats, conditions that were improved by apocyni

54 ersus 72+/-3%, P<0.05) were also impaired in DOCA-salt.

55 teric arteries was significantly improved in DOCA-salt-treated Tg-GCH mice, in parallel with reduced

56 w endothelin-1 (ET-1), which is increased in DOCA-salt hypertensive rats, contributes to arterial sup

57 ide (NK3r agonist) attenuates salt intake in DOCA-treated animals.

58 re we examined whether CXCL16 is involved in DOCA-salt-induced renal inflammation and fibrosis.

59 decreased GTPCH I activity and BH4 levels in DOCA-salt compared with sham rats.

60 for the increased renal production of NO in DOCA-salt hypertension, and are consistent with a role f

61 ared with sham controls but was preserved in DOCA-salt-treated Tg-GCH mice.

62 itant decrease of systolic blood pressure in DOCA-salt rats.

63 ling; all of these effects were prevented in DOCA-salt-treated Tg-GCH mice.

64 r endothelium-dependent vessel relaxation in DOCA-salt rats, excluding a role of a local renin/angiot

65 dependent relaxation and basal NO release in DOCA-salt rats.

66 ation and lipid accumulation were studied in DOCA-salt treated rats.

67 0beta protein density, but neither L-NNA nor DOCA-salt had differences in p85alpha and p110alpha.

68 ignificantly elevated in carotid arteries of DOCA-salt rats compared with that of the sham-operated c

69 Treatment of arteries of DOCA-salt rats with the selective ETA receptor antagonis

70 sed superoxide levels in carotid arteries of DOCA-salt rats.

71 dothelial dysfunction in carotid arteries of DOCA-salt rats.

72 eated them with a range of concentrations of DOCA and found a dose-dependent decrease in NK3r-mRNA ab

73 n (SFO); are required for the development of DOCA-salt hypertension.

74 al convoluted tubule (DCT) in the kidneys of DOCA-salt mice and CD8(+) T cell-injected mice, leading

75 Treatment of DOCA-salt rats with serelaxin decreased renal inflammati

76 During 3 weeks of DOCA-salt treatment, arterial blood pressure was increas

77 e uninephrectomized, and either a placebo or DOCA pellet was implanted subcutaneously.

78 relaxation, tau, improving with ranolazine (DOCA-salt, 0.18 +/- 0.02, DOCA-salt+ranolazine, 0.13 +/-

79 In summary, serelaxin reversed DOCA-salt induced cardiac and renal dysfunction.

80 mice with deoxycorticosterone acetate-salt (DOCA-salt) hypertension, ROS production from NO synthase

81 t diet and deoxycorticosterone acetate-salt (DOCA-salt) treatments, but BP control remained intact.

82 receptors are downregulated after subchronic DOCA treatment and this finding is consistent with the h

83 TAC/DOCA cRbm20(DeltaRRM)-DMSO mice developed LV hypertrophy

84 LV chamber stiffness was normalized in TAC/DOCA cRbm20(DeltaRRM)-raloxifene mice that expressed N2B

85 ant improvement in exercise tolerance in TAC/DOCA mice that expressed N2BAsc.

86 was equally increased in both groups of TAC/DOCA mice (cRbm20(DeltaRRM)-DMSO and cRbm20(DeltaRRM)-ra

87 c function and exercise tolerance in the TAC/DOCA model.

88 in a renovascular model of hypertension, the DOCA-salt rat, and if these changes are preventable by n

89 Oxidative stress in the DOCA-salt model may increase late I(Na), resulting in di

90 required for hypertension development in the DOCA-salt model.

91 After 4 weeks, the DOCA-salt rats were randomly selected and implanted with

92 blunts the increase in blood pressure due to DOCA-salt hypertension.

93 ecovery of PGC-1alpha expression response to DOCA-salt challenge in offspring that underwent prenatal

94 infiltration into the kidneys in response to DOCA-salt hypertension.

95 minuria and glomerular damage in response to DOCA.

96 dividual contribution of these structures to DOCA-salt hypertension is unknown.

97 io, was decreased significantly in wild-type DOCA-salt mice compared with sham controls but was prese

98 ly 100-microm outside diameter) in wild-type DOCA-salt mice exists, evidenced by increased medial cro

99 ls were decreased significantly in wild-type DOCA-salt mice, but both were preserved in Tg-GCH mice d

100 versus sham+ranolazine, 0.18 +/- 0.01 versus DOCA-salt, 0.23 +/- 0.2 versus DOCA-salt+ranolazine, 0.1

101 - 0.01 versus DOCA-salt, 0.23 +/- 0.2 versus DOCA-salt+ranolazine, 0.17 +/- 0.0 1 mm Hg/L; P<0.005).

102 To examine whether DOCA's effects on NK3r synthesis are direct, we used dif

103 ly minimally altered in vessels of mice with DOCA-salt hypertension but seems to be mediated by hydro

104 normal drinking water and DOCA provided with DOCA pellets and sodium chloride drinking water.

105 Thus, we injected rats with DOCA once daily for 11 days and analyzed tachykinin rece

106 Rats were treated with DOCA and saline drinking water for 3 weeks.

107 ression of hypertension in mice treated with DOCA-salt.