Salt-induced exacerbation of morning surge in blood pressure in patients with essential hypertension

Osanai, Tomohiro; Okuguchi, Tomoyuki; Kamada, T.; Fujiwara, Nozomi; Kosugi, Takuo; Saitoh, Genta; Katoh, Takeshi; Nakano, Takao; Takahashi, Kazunori; Guan, Wutai; Okumura, Ken

doi:10.1038/sj.jhh.1000945

Cited by 31 publications

(34 citation statements)

References 24 publications

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“…2 We further showed that salt-sensitive hypertension manifests an absent or decreased nocturnal reduction in blood pressure, 30 and nondippers, ie, patients with an absent or decreased nocturnal reduction in their blood pressure, tend to have more severe target-organ damage than do dippers, ie, those with a normal nocturnal decrease in blood pressure. 31 Furthermore, a prospective study demonstrated that cardiovascular morbidity was higher in nondippers than in dippers, 32 indicating that ADMA release by shear stress might contribute to the occurrence of cardiovascular events in human hypertension.…”

Section: Discussionmentioning

confidence: 99%

Effect of Shear Stress on Asymmetric Dimethylarginine Release From Vascular Endothelial Cells

et al. 2003

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Abstract-We demonstrated recently that plasma concentrations of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthase, are increased by high salt intake concomitantly with a decrease in plasma levels of NO in human hypertension. We investigated the effect of shear stress on ADMA release in 2 types of cells: transformed human umbilical vein endothelial cells (HUVECs; cell line ECV-304) and HUVECs. Exposure of ECV-304 cells and HUVECs to shear stress with the use of a cone-plate viscometer enhanced gene expression of protein arginine methyltransferase (PRMT-1), ADMA synthase. In HUVECs, the ratio of PRMT-1 to glyceraldehyde 3-phosphate dehydrogenase mRNA was increased by 2-fold by a shear stress of Ն15 dyne/cm 2 . A dominant-negative mutant of IB kinase ␣ and troglitazone at 8 mol/L, an activator of peroxisome proliferator-activated receptor ␥, abolished the shear stress-induced increase in PRMT-1 gene expression in parallel with the blockade of nuclear factor (NF)-B translocation into the nucleus. The activity of dimethylarginine dimethylaminohydrolase, the degradation enzyme of ADMA, was unchanged after shear stress Յ15 dyne/cm 2 and was enhanced by 1.48Ϯ0.06-fold (PϽ0.05) by shear stress at 25 dyne/cm 2 . The release of ADMA was increased by 1.64Ϯ0.10-fold (PϽ0.05) by shear stress at 15 dyne/cm 2 but was not affected by shear stress at 25 dyne/cm 2 . These results indicate that shear stress enhances gene expression of PRMT-1 and ADMA release via activation of the NF-B pathway. Shear stress at higher magnitudes facilitates the degradation of ADMA, thus returning ADMA release levels to baseline. Key Words: stress, mechanical Ⅲ endothelium Ⅲ gene expression Ⅲ arginine Ⅲ nitric oxide Ⅲ nitric oxide synthase N itric oxide (NO) contributes to vessel homeostasis by inhibiting vascular smooth muscle tone and growth, platelet aggregation, and leukocyte adhesion to the endothelium. 1 Altered biosynthesis of NO has been implicated in the pathogenesis of atherosclerosis, and it is possible that accumulation of endogenous asymmetric dimethylarginine (ADMA), an endogenous competitive inhibitor of NO synthase (NOS), underlies the reduced NO generation. We demonstrated recently that a high salt intake decreases the plasma concentrations of nitrite and nitrate (NO x ) concomitantly with an increase in plasma concentrations of ADMA in patients with essential hypertension. 2 A high salt intake causes a number of physiologic and pathologic effects, such as hemodynamic modulation, increased activity of the reninangiotensin-aldosterone system, and activation of the sympathetic nerve system. High salt intake-induced hemodynamic modulation includes augmentation of shear stress to the vascular wall, especially to endothelial cells, and we hypothesized that a high salt intake-induced decrease in plasma NO x levels might be caused by a shear stress-induced elevation of circulating ADMA.Vascular endothelial cells are capable of synthesizing ADMA, which is derived from the catabolism of proteins containi...

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Section: Discussionmentioning

confidence: 99%

Effect of Shear Stress on Asymmetric Dimethylarginine Release From Vascular Endothelial Cells

et al. 2003

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“…Salt sensitivity is an insidious “silent killer” since even in individuals with normal blood pressure it can lead to cardiovascular morbidity and mortality (3) and is associated with other diseases, e.g., asthma (4), gastric carcinoma (5), osteoporosis (6), and renal dysfunction (7), among others. High sodium intake can aggravate the morning surge of blood pressure even in salt-resistant subjects (8) that could be associated with increased cardiovascular risk, in some studies (9). Although some studies suggest that non-dipping hypertension associated with low morning surge could also be associated with decreased cardiovascular risk (10), high sodium intake is also associated with non-dipping hypertension which is associated with increased cardiovascular risk (11).…”

Section: Introductionmentioning

confidence: 99%

The renal dopaminergic system: novel diagnostic and therapeutic approaches in hypertension and kidney disease

Armando

Konkalmatt

Felder

et al. 2015

Translational Research

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Salt sensitivity of blood pressure, whether in hypertensive or normotensive subjects, is associated with increased cardiovascular risk and overall mortality. Salt sensitivity can be treated by reducing NaCl consumption. However, decreasing salt intake in some may actually increase cardiovascular risk, including an increase in blood pressure, i.e., inverse salt sensitivity. Several genes have been associated with salt sensitivity and inverse salt sensitivity. Some of these genes encode proteins expressed in the kidney that are needed to excrete a sodium load, e.g., dopamine receptors and their regulators, GRK4. We review here research in this field that has provided several translational opportunities, ranging from diagnostic tests to gene therapy, such as: 1) a test in renal proximal tubule cells isolated from the urine of humans that may determine the salt-sensitive phenotype by analyzing the recruitment of dopamine D1 receptors to the plasma membrane; 2) presence of common GRK4 gene variants that are not only associated with hypertension but may also be predictive of the response to antihypertensive therapy; 3) genetic testing for polymorphisms of the dopamine D2 receptor that may be associated with hypertension and inverse salt sensitivity and may increase the susceptibility to chronic kidney disease because of loss of the anti-oxidant and anti-inflammatory effects of the renal dopamine D2 receptor, and 4) in vivo renal selective amelioration of renal tubular genetic defects by a gene transfer approach, using AAV vectors introduced to the kidney by retrograde ureteral infusion.

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“…[22][23][24] Recent reports suggest that morning surge is closely related to incidence of cardiovascular and cerebrovascular diseases. 25,26 Blood pressure and salt intake differ in individuals and on different days. Thus, it would be useful to measure morning blood pressure and salt intake with the new salt monitor and to examine the relationship between blood pressure and salt intake for a relatively long period.…”

Section: Introductionmentioning

confidence: 99%

Self-monitoring of home blood pressure with estimation of daily salt intake using a new electrical device

Yamasue

Tochikubo

Kono³

et al. 2006

J Hum Hypertens

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We investigated a simple device to monitor daily salt intake at home and examined the relationship between salt excretion and morning blood pressure in order to enable patients to better manage daily salt intake and hypertension. The correlation between 24-h urinary salt excretion and measured value with salt monitor from overnight urine was significant (n ¼ 224, r ¼ 0.72, Po0.001). A total of 46 volunteers participated for more than 3 weeks by measuring daily salt intake and morning blood pressure. The relationship between predicted daily salt excretion and blood pressure was examined with use of 3-day moving average. Mean salt excretion and systolic blood pressure (SBP) significantly decreased by the end of the trial (i.e., salt excretion decreased from 158731 to 149730 mmol/day and SBP from 137717 to 133716 mm Hg). Of 46 participants, 18 (39%) had a significant correlation between predicted daily salt excretion and blood pressure (r40.4, Po0.05, n421), indicating sodium sensitivity. An additional 17% had a positive correlation that did not reach statistical significance (0.2orp0.4), and the remaining 44% had no correlation (rp0.2). Mean decrease in blood pressure per decrease in salt (g) (17 mmol) intake in the 18 participants with a significant correlation was 3.3 mm Hg (SBP) and 1.5 mm Hg (diastolic blood pressure), which was higher than that reported for other studies. Hypertensive patients not using medication showed the largest decrease. We conclude that daily monitoring of salt intake and morning blood pressure will be useful for management of hypertension.

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Salt-induced exacerbation of morning surge in blood pressure in patients with essential hypertension

Cited by 31 publications

References 24 publications

Effect of Shear Stress on Asymmetric Dimethylarginine Release From Vascular Endothelial Cells

Effect of Shear Stress on Asymmetric Dimethylarginine Release From Vascular Endothelial Cells

The renal dopaminergic system: novel diagnostic and therapeutic approaches in hypertension and kidney disease

Self-monitoring of home blood pressure with estimation of daily salt intake using a new electrical device

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