ライフサイエンスコーパス: salt intake

1 regulation of insulin sensitivity to dietary salt intake.

2 al P-450 isoform regulated by excess dietary salt intake.

3 c) were studied for BP response to increased salt intake.

4 precede the hypertension resulting from high salt intake.

5 tenance of normal blood pressure during high salt intake.

6 in mice and humans across various levels of salt intake.

7 y involved in the vascular responses to high salt intake.

8 ly consumed processed pork products to total salt intake.

9 d with health outcomes obtained with current salt intake.

10 reby influencing BP under conditions of high salt intake.

11 in rats during sodium deprivation and after salt intake.

12 ring various ingestive activities, including salt intake.

13 n calcium retention as a function of dietary salt intake.

14 neration increased (P < 0.05) 30 to 40% with salt intake.

15 that was independent of the level of dietary salt intake.

16 were challenged to a normal- or chronic high-salt intake (1% NaCl).

17 In populations with high salt intake, a modest reduction in salt intake lowers bl

18 one of the mechanisms underlying how dietary salt intake affects the activity of VP neurons via ENaC

19 Here we show that high salt intake affects the gut microbiome in mice, particul

20 eted subjects displayed significantly larger salt intakes after their second experience with sodium d

21 ension produced by the combination of a high salt intake and administration of angiotensin II, the An

22 consistently shown a direct relation between salt intake and cardiovascular risk, and a reduction in

23 ciation with an inverse relationship between salt intake and heart rate, indicating intact barorecept

24 observations regarding the relation between salt intake and its reduction on blood pressure have eme

25 endocrine mechanisms that regulate water and salt intake and loss.

26 oordinating homeostatic responses to dietary salt intake and suggest a complex pathophysiology for hy

27 The relationship between dietary salt intake and the associated risk of hypertension and

28 a(+)] and osmolality rise in proportion with salt intake and thus promote release of vasopressin (VP)

29 distribution of risk factors associated with salt intake and tobacco use, and to model the effects on

30 SRA mice exhibited an increase in water and salt intake and urinary volume, which were significantly

31 ntly increased-183% by losartan, 212% by low salt intake, and 227% by the combination of the two-comp

32 ndocrine secretion, cardiovascular function, salt intake, and nociception.

33 youngest vs. oldest: 24% vs. 7%, p = 0.001), salt intake, and other dietary measures (21% vs. 9%, p =

34 elevated plasma angiotensin II and increased salt intake (AngII-salt).

35 r pylori (H. pylori) infection and excessive salt intake are known as important risk factors for stom

36 The cardiovascular benefits of reduced salt intake are on par with the benefits of population-w

37 cobacter pylori infection and a high dietary salt intake are risk factors for the development of gast

38 ake, studies specifically designed to assess salt intake as an endpoint are needed.

39 ally involved in the control of need-induced salt intake; (b) negative feedback from the stomach and

40 ered on what basis (eg, sex, ethnicity, age, salt intake, baseline renin, ACE or aldosterone, and gen

41 ly marginal, if any, effects of amiloride on salt intake behavior, highlighting the importance of con

42 eceptors were significantly increased by low salt intake but were significantly decreased by losartan

43 sources of sodium to reduce adult population salt intake by approximately 30% toward the optimal WHO

44 neuroanatomical basis for the modulation of salt intake by the CeA.

45 Also after salt intake, c-Fos activation increased within pontine n

46 mation regarding the feasibility of reducing salt intake, call for renewed efforts in this area as a

47 gy, we examine evidence that the lowering of salt intake can combat hypertension.

48 els that may occur in human blood after high-salt intake can potentiate, in serum-free culture condit

49 In decoy rats, high salt intake caused a greater positive sodium balance.

50 We show that high dietary salt intake caused an increase in the expression and act

51 Dietary salt intake controls epithelial Na+ channel (ENaC)-media

52 A 6-g/d increase in salt intake decreased the level of rhythmical mineraloco

53 e unexpected observation that long-term high salt intake did not increase water consumption in humans

54 Mice with high dietary salt intake display enhanced induction of Th17 response

55 zed clinical and MRI follow-up, suggest that salt intake does not influence MS disease course or acti

56 Thus, salt intake enhances generation of O(2)(.-) accompanied

57 After 4 weeks of high-salt intake, ES rats still showed a lower mean serum cre

58 id not decrease food intake after fasting or salt intake following salt depletion; inactivation incre

59 High dietary salt intake for 7 days caused an increase in expression

60 On the normal salt intake for the UK population, supine blood pressure

61 Across all 3 levels of salt intake, half-weekly and weekly rhythmical mineraloc

62 Excessive salt intake has been associated with hypertension and in

63 Hyperosmolality due to high dietary salt intake has been linked to pathological inflammatory

64 rmine how, in the face of chronic changes in salt intake, humans maintain volume and osmotic homeosta

65 Here we show that chronic high salt intake impairs baroreceptor inhibition of rat VP ne

66 ection of senktide (NK3r agonist) attenuates salt intake in DOCA-treated animals.

67 time that 20-HETE excretion is regulated by salt intake in hypertension.

68 from the home would reduce total population salt intake in New Zealand by 35% (from 8.4 to 5.5 g/d)

69 otective in the setting of low sugar and low salt intake in our past, today, the combination of diets

70 he amygdala (CeA) has been shown to modulate salt intake in response to aldosterone, so we investigat

71 We selected two interventions: to reduce salt intake in the population by 15% and to implement fo

72 on observed in response to increased dietary salt intake in these animals.

73 A 6-g/d increase in salt intake increased urine osmolyte excretion, but redu

74 The idea that increasing salt intake increases drinking and urine volume is widel

75 We show that high salt intake increases the spontaneous firing rate of VP

76 rone-acetate (DOCA) in combination with high salt intake induced arterial hypertension of similar mag

77 Excess dietary salt intake induces the activity of the kidney arachidon

78 roaches we tested whether increased maternal salt intake influences fetal kidney development to rende

79 ate that osmotic balance in response to high salt intake involves a complex regulatory process that i

80 High salt intake is a major risk factor for hypertension.

81 nance of osmotic balance in response to high salt intake is a passive process that is mediated largel

82 logical studies have shown that high dietary salt intake is also a risk factor for gastric cancer.

83 Salt intake is an established response to sodium deficie

84 vascular risk, and a reduction in population salt intake is associated with a reduction in cardiovasc

85 Reducing salt intake is considered an important public health str

86 ies, support the judgment that habitual high salt intake is one of the quantitatively important, prev

87 dy was to examine whether changes in dietary salt intake lead to compensatory changes in expression o

88 A modest reduction in salt intake leads to a fall in blood pressure in both no

89 High salt intake leads to high blood pressure, even when occu

90 e feeding of HCl in the presence of a normal salt intake led to a degree of metabolic acidosis not si

91 r surplus reduced fluid intake at the 12-g/d salt intake level.

92 ys' duration, we exposed 10 healthy men to 3 salt intake levels (12, 9, or 6 g/d).

93 INTERSALT showed that high salt intake, low potassium intake, excess alcohol consum

94 with high salt intake, a modest reduction in salt intake lowers blood pressure and diminishes cardiov

95 ed blood pressure, and a modest reduction in salt intake lowers blood pressure, which is predicted to

96 ation in mice and in humans and that chronic salt intake may exacerbate gastritis by increasing H. py

97 Furthermore, elevated salt intake may potentiate H. pylori-associated carcinog

98 d 5.8% of stroke cases might be prevented if salt intake meets the recommended maximum intake.

99 Thus, increased dietary salt intake might represent an environmental risk factor

100 Lifelong environmental factors (eg, salt intake, obesity, alcohol) and genetic factors clear

101 r six risk factors (tobacco and alcohol use, salt intake, obesity, and raised blood pressure and gluc

102 r six risk factors (tobacco and alcohol use, salt intake, obesity, and raised blood pressure and gluc

103 ervention designed to achieve a reduction in salt intake of 3 g per day would save 194,000 to 392,000

104 We tested the hypothesis that an increase in salt intake of 6 g/d would change fluid balance in men l

105 and 3) adherence to the recommended maximum salt intake of 6 g/d.

106 ction with slow sodium and placebo to give a salt intake of either 10 g (equivalent to the normal amo

107 Compelling evidence of the role of salt intake on blood pressure and on other risk factors

108 nt study, we evaluated the effect of dietary salt intake on ENaC regulation and activity in VP neuron

109 a systematic study of the effects of dietary salt intake on glomerular filtration rate (GFR) and tubu

110 l and observational studies on the effect of salt intake on renal and cardiovascular outcomes.

111 ly to the effect of dietary sodium chloride (salt) intake on BP.

112 here are no data on regulation of 20-HETE by salt intake or on a role for this compound in SS hyperte

113 tion, nor do they justify advice to increase salt intake or to decrease its concentration in the diet

114 ficantly elevated by losartan treatment, low salt intake, or a combination of the two, compared with

115 creased incrementally two- to threefold with salt intake (P < 0.001), whereas prostaglandin E(2) was

116 Increased dietary salt intake promotes an early and uniform expansion of e

117 t alternatives would lead to slightly higher salt intake reductions and thus to more health gain.

118 Thus, sodium deficiency and salt intake stimulate separate subpopulations of neurons

119 valuate the mechanisms and safety of reduced salt intake, studies specifically designed to assess sal

120 During high-salt intake, the sik1(+/+) mice exhibited an increase in

121 blood pressure development triggered by high-salt intake through the modulation of the contractile ph

122 data suggest that animals exposed to chronic salt intake to a level close to that reported for human'

123 To review the evidence that relates salt intake to blood pressure and cardiovascular disease

124 An increase in salt intake to greater than or equal to 3.0% NaCl increa

125 Our results connect high salt intake to the gut-immune axis and highlight the gut

126 lth outcomes were obtained in 2 steps: after salt intake was modeled into blood pressure levels, the

127 Higher salt intake was not associated with decreased time to re

128 Salt intake was reported to be associated with increased

129 Increased physical activity, a reduced salt intake, weight loss, moderation of alcohol intake,

130 ional interventions, especially reduction of salt intake, which is rather high in the Western world.