Enhanced sodium sensitivity and disturbed circadian rhythm of blood pressure in essential hypertension

Uzu, Takashi; Kimura, Genjiro; Yamauchi, Atsushi; Kanasaki, Megumi; Isshiki, Keiji; Araki, Shin‐ichi; Sugiomoto, Toshiro; Nishio, Yoshihiko; Maegawa, Hiroshi; Koya, Daisuke; Haneda, Masakazu; Kashiwagi, Atsunori

doi:10.1097/01.hjh.0000239299.71001.77

Cited by 119 publications

(98 citation statements)

References 30 publications

(38 reference statements)

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“…[1][2][3][4][5] Although the pathogenesis of salt sensitivity is unknown, both genetic and environmental factors appear to interact to determine the exaggerated BP response to changes in salt intake. [6][7][8][9][10][11][12][13][14][15] Increased reactivity of BP to salt is commonly observed in subjects with obesity and associated cardiovascular risk factors. [6][7][8][9][10] Insulin resistance, hypertension, increased sympathetic activity, endothelial dysfunction and abnormal nitric oxide (NO) bioactivity are among the list of factors that have been proposed to directly or indirectly lead to salt sensitivity related to obesity.…”

Section: Introductionmentioning

confidence: 99%

Effects of lifestyle changes and metformin on salt sensitivity and nitric oxide metabolism in obese salt-sensitive Hispanics

2007

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Salt sensitivity is associated with obesity, and increased cardiovascular morbidity and mortality. We investigated whether treatment of obesity and its associated metabolic abnormalities corrects salt sensitivity and restores impaired nitric oxide (NO) metabolism characteristic of salt sensitivity. Twenty, otherwise, healthy obese saltsensitive subjects completed a 12-month program of caloric restriction, aerobic exercise and metformin. Two salt sensitivity tests were performed, that is at baseline and end of program. Lifestyle-metformin treatment decreased weight (9.870.3 kg), body mass index (3.970.2 kg/m 2 ), waist (11.570.5 cm), systolic blood pressure (SBP) (8.670.4 mm Hg), diastolic blood pressure (DBP) (5.570.4 mm Hg), triglyceride (4075 mg/dl), fasting (8.371 lIU/ml) and post-load (2074 lIU/ml) insulin levels, and salt sensitivity. Going from a highsodium (B300 mmol) to a low-sodium diet (B30 mmol of sodium/day) lowered SBP/DBP by 14.771.7/7.470.9 mm Hg at baseline and by 8.671.9/3.271.2 mm Hg after treatment (Po0.001). More importantly, blood pressure (BP) sensitivity to customary levels of dietary salt (B150 mmol of sodium/day) was abolished by the lifestyle-metformin treatment. Differences in SBP/DBP between usual and low salt averaged 1171/871 mm Hg before treatment, and 371/170.5 mm Hg after treatment (Po0.001). At baseline, NO-metabolite excretion was inhibited during high salt; this impairment was corrected by the lifestyle-metformin treatment. In conclusion, acquired correctable factors play an important role in the pathogenesis of salt sensitivity associated with obesity. Correction of salt sensitivity may account for the BP lowering induced by weight reduction. Restoration of the inability to increase or sustain NO production in response to high salt could account for the correction of salt sensitivity induced by the lifestylemetformin treatment.

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Section: Introductionmentioning

confidence: 99%

Effects of lifestyle changes and metformin on salt sensitivity and nitric oxide metabolism in obese salt-sensitive Hispanics

2007

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“…Earlier data have also provided evidence that there might be an inter-relationship between MetS, enhanced sodium sensitivity of the blood pressure and non-dipping pattern. 9 Little is known about the relationship between the circadian profile of blood pressure, dipping pattern and insulin, as well as glucose metabolism in subjects without any known metabolic diseases. Therefore, we investigated the possible association between 24-h blood pressure profile and glucose tolerance status, MetS, as well as its components in a large population-based cohort (n¼462) without diagnosed hypertension or diabetes.…”

Section: Introductionmentioning

confidence: 99%

Non-dipping pattern in ambulatory blood pressure monitoring is associated with metabolic abnormalities in a random sample of middle-aged subjects

2009

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A reduction in the blood pressure decline at night (o10% from daytime systolic blood pressure (SBP)) during 24-h ambulatory blood pressure monitoring (ABPM) ('non-dipping pattern') is associated with cardiovascular morbidity. Our aim was to evaluate whether ABPM characteristics are associated with metabolic abnormalities in subjects without known hypertension or type 2 diabetes mellitus (T2DM). This is a cross-sectional population-based study on middle-aged subjects (n¼462). Two distinct definitions of metabolic syndrome (MetS) were used: National Cholesterol Education Program-Third Adult Treatment Panel (NCEP-ATPIII) and International Diabetes Federation (IDF) criteria. Results suggested that subjects characterized by non-dipping in 24 h ABPM were more obese (P¼0.014). After adjustment for body mass index, age and sex, non-dippers had higher verylow-density lipoprotein (VLDL)-cholesterol (P¼0.003), total (P¼0.029)-and VLDL-triglycerides (P¼0.026) and oral glucose tolerance test 2 h blood glucose (P¼0.027) compared with dippers. Non-dipping status was more common among subjects with MetS (Pp0.01), impaired glucose tolerance (IGT) (Po0.05) and in those with the combination of IGT-T2DM (Pp0.01) than among those without these abnormalities. ABPM non-dipping status was an independent predictor of IGT in multivariate models (Po0.05). With respect to MetS components, high triglycerides (Pp0.005) and low high density lipoprotein-cholesterol (Po0.05) were associated with a non-dipping pattern. The percentage decline in blood pressure from day to night decreased with the number of metabolic abnormalities (P¼0.012). In conclusion, ABPM non-dipping status is an independent predictor of glucose intolerance. It is also associated with several other metabolic abnormalities. Whether non-dipping pattern is causally related to these metabolic aberrations remains to be explored in a future prospective follow-up of this cohort.

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“…However, several other neurohormonal systems regulating BP have been shown to follow a circadian rhythm and may contribute to the circadian variations in BP. 11,12 Some studies have suggested that the reduction or even the inversion of the usual nocturnal dipping in some subjects is associated with high sodium intake and salt sensitivity [13][14][15][16][17] . Recently, Fukuda et al 18 proposed a hypothesis according to which the nondipping pattern of BP at night is because of an impaired capacity to excrete sodium during daytime.…”

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confidence: 99%

Nighttime Blood Pressure and Nocturnal Dipping Are Associated With Daytime Urinary Sodium Excretion in African Subjects

et al. 2008

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Abstract-Blood pressure (BP) follows a circadian rhythm, with 10% to 15% lower values during nighttime than during daytime. The absence of a nocturnal BP decrease (dipping) is associated with target organ damage, but the determinants of dipping are poorly understood. We assessed whether the nighttime BP and the dipping are associated with the circadian pattern of sodium excretion. Ambulatory BP and daytime and nighttime urinary electrolyte excretion were measured simultaneously in 325 individuals of African descent from 73 families. When divided into sex-specific tertiles of day:night ratios of urinary sodium excretion rate, subjects in tertile 1 (with the lowest ratio) were 6.5 years older and had a 9.8-mm Hg higher nighttime systolic BP (SBP) and a 23% lower SBP dipping (expressed in percentage of day value) compared with subjects in tertile 3 (P for trend Ͻ0.01). After adjustment for age, the SBP difference across tertiles decreased to 5.4 mm Hg (Pϭ0.002), and the SBP dipping difference decreased to 17% (Pϭ0.05). A similar trend across tertiles was found with diastolic BP. In multivariate analyses, daytime urinary sodium and potassium concentrations were independently associated with nighttime SBP and SBP dipping (PϽ0.05 for each). These data, based on a large number of subjects, suggest that the capacity to excrete sodium during daytime is a significant determinant of nocturnal BP and dipping. This observation may help us to understand the pathophysiology and clinical consequences of nighttime BP and to develop therapeutic strategies to normalize the dipping profile in hypertensive patients. (Hypertension. 2008;51:891-898.)

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Enhanced sodium sensitivity and disturbed circadian rhythm of blood pressure in essential hypertension

Cited by 119 publications

References 30 publications

Effects of lifestyle changes and metformin on salt sensitivity and nitric oxide metabolism in obese salt-sensitive Hispanics

Effects of lifestyle changes and metformin on salt sensitivity and nitric oxide metabolism in obese salt-sensitive Hispanics

Non-dipping pattern in ambulatory blood pressure monitoring is associated with metabolic abnormalities in a random sample of middle-aged subjects

Nighttime Blood Pressure and Nocturnal Dipping Are Associated With Daytime Urinary Sodium Excretion in African Subjects

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