Significance of sympathetic nervous system in sodium-induced nocturnal hypertension

Okuguchi, Tomoyuki; Osanai, Tomohiro; Kamada, Takaatsu; Kimura, Masao; Takahashi, Koki; Okumura, Ken

doi:10.1097/00004872-199917070-00011

Cited by 20 publications

(16 citation statements)

References 33 publications

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“…We demonstrated recently that a high salt intake increases the plasma concentration of ADMA and decreases that of NO x in patients with salt-sensitive essential hypertension. 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: 97%

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: 97%

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

et al. 2003

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“…Our findings also pattern studies of patients with essential hypertension where blood pressure fails to fall during rest when the subject is on a high NaCl diet and exhibits a salt-sensitive form of hypertension. This finding in humans was associated with a loss of the circadian pattern of plasma norepinephrine (21), which may imply a failure of circadian variation in sympathetic nervous system activity. Because the present WKY/lj-tf and WKY/lj-cr rats both exhibit decreases in daytime arterial pressure and SHR/lj-cr lack the ability to attenuate the pressor effects of high NaCl during rest, the allelic differences among the strains may facilitate identifying those genes that contribute to this failure in regulation.…”

Section: Discussionmentioning

confidence: 93%

A new inbred Wistar-Kyoto rat substrain exhibiting apparent salt sensitivity and borderline hypertension

Alemayehu

Breen

Printz

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Alemayehu, Adamu, Laura Breen, and Morton P. Printz. A new inbred Wistar-Kyoto rat substrain exhibiting apparent salt sensitivity and borderline hypertension. Am J Physiol Heart Circ Physiol 283: H1181-H1190, 2002. First published May 23, 2002 10.1152/ajpheart.00187.2002The normotensive Wistar-Kyoto (WKY) rat strain is a traditional control for the spontaneously hypertensive rat (SHR). We found trait differences between two inbred normotensive WKY strains, derived originally from different vendors, and compared these two strains from La Jolla-Taconic Farms (WKY/lj-tf) and La Jolla-Charles River (WKY/lj-cr) with the inbred SHR/lj-cr for cardiovascular, diurnal, and activity traits under normal and high (8%) NaCl diets. Marked genetic diversity was found between the two vendor-derived WKY. By using an extended study design and radiotelemetry, we compared WKY/lj-cr, WKY/lj-tf, and SHR/lj-cr with the following results: systolic pressure (120 Ϯ 1, 133 Ϯ 1, 168 Ϯ 3 mmHg, respectively); diurnal variation in heart rate (⌬HR: 46 Ϯ 3, 71 Ϯ 4, 57 Ϯ 2 beats/min, respectively); and salt sensitivity of arterial pressure (⌬systolic: 10 Ϯ 1, 21 Ϯ 1, 20 Ϯ 1 mmHg, respectively). The WKY/lj-tf genotype apparently results in compromised control of arterial pressure and heart rate, especially during high NaCl intake, and greater susceptibility to high pressure (i.e., high NaCl-induced secondary changes). WKY/lj-tf thus constitutes a new inbred borderline hypertensive WKY substrain offering unique opportunities for genomic studies into the development of genetic hypertension. inbred strains; hypertension sodium-dependent; genotype; circadian rhythm; radiotelemetry; heart rate; polymorphism MOST INVESTIGATORS have been using descendants of the normotensive Wistar-Kyoto (WKY) rat strain as the control for the Okamoto and Aoki (20) spontaneously hypertensive rat (SHR). As a result of both highly inbred original stock and standardized breeding practices, virtual uniformity has resulted in the SHR supplied by major commercial vendors (5). However, the rigorous procedures applied to the initial inbreeding and subsequent distribution of the SHR were not used for the WKY rat derived after the SHR. As a result, animals were distributed to commercial suppliers as early as the 10th generation of inbreeding (13). Furthermore, subsequent breeding was not standardized with some suppliers (including Charles River Laboratories) maintaining brother-sister matings (10) to sustain the founder stock, whereas others (including Taconic Farms) used a random breeding (outbred) protocol (26).Studies from several laboratories, including our own, compared WKY rats from Charles River Laboratories (WKY/cr; Wilmington, MA) and Taconic Farms (WKY/ tf; Germantown, NY) and reported pronounced trait differences (9,13,14,24). Our own laboratory (8), as early as 1984, noted differences in 1) consummatory behaviors including an enhanced salt preference in WKY/tf, 2) age-weight relationships, and 3) cardiovascular traits between these WKY substrains. Furthermore, we rep...

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“…Sodium sensitivity is affected by such factors as defects in renal sodium excretion (37), abnormally weak suppression of intrarenal renin release (38), paradoxical decrease in atrial natriuretic peptide secretion (39), and decreased renal-kallikrein activity (40). Moreover, increased sympathetic nervous system activity (12,13,41) and pressor reactivity (42) may play a large role in this phenomenon. On the other hand, Grassi et al (43) reported that moderate dietary sodium restriction triggers sympathetic activation, and Minami et al (44) also reported that a high-sodium diet decreased LF/HF in non-sodium-sensitive hypertensive patients.…”

Section: Discussionmentioning

confidence: 99%

“…It has been proposed that accentuation of sympathetic nervous system activity or cardiac sympatho-vagal imbalance may contribute to sodium sensitivity (12,13). The present study investigated the relations among three factors in a group of young men: sleep-BP (base-BP) (3), Salt24, and cardiac sympatho-vagal balance (SVB).…”

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confidence: 95%

“…To evaluate whether 24-h urine had been collected correctly, we determined the correlation between lean body mass (LBM) measured according to the impedance method and 24-h urinary creatinine excretion (Cr24), and excluded data that fell outside the 95% confidence limits of the linear relationship between Cr24 and LBM (16). We have previously reported the accuracy of these measurements (12)(13)(14)(15)(16)(17). Salt24 was obtained by dividing the 24-h urinary Na excretion value (mmol/day) by 17.1 (mmol/g).…”

Section: Introductionmentioning

confidence: 99%

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Sodium Intake and Cardiac Sympatho-Vagal Balance in Young Men with High Blood Pressure

Tochikubo¹,

Nishijima²

2004

Hypertens Res

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Significance of sympathetic nervous system in sodium-induced nocturnal hypertension

Abstract: BP fails to fall during the night under the high-salt diet in patients with the SS type of essential hypertension. This may be related to the lack of nocturnal decrease in sympathetic nervous activity.

Cited by 20 publications

References 33 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

A new inbred Wistar-Kyoto rat substrain exhibiting apparent salt sensitivity and borderline hypertension

Sodium Intake and Cardiac Sympatho-Vagal Balance in Young Men with High Blood Pressure

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