著者

Yukio YAMORI Longjian LIU Katsumi IKEDA Ayako MIURA Shunsaku MIZUSHIMA Tomohiro MIKI Yasuo NARA on Behalf of the WHO-Cardiovascular Disease and Alimentary Comparison (CARDIAC) Study Group

出版者

The Japanese Society of Hypertension

雑誌

Hypertension Research (ISSN:09169636)

巻号頁・発行日

vol.24, no.4, pp.453-457, 2001 (Released:2002-03-29)

参考文献数

18

被引用文献数

89 111

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There is considerable interest in the association between taurine (2-aminoethanesufonic acid) and risk of ischemic heart disease (IHD), but little information has been made available on the distribution of taurine in populations around the world. The present study aimed to describe the differences in taurine excretion levels and their associations with IHD mortality rates in 24 populations in 16 countries worldwide. This was a multicenter cross-sectional study. In each center, 100 men and 100 women aged 48-56 years were selected randomly from the local populations. Twenty-four hour urinary taurine excretion was measured using an amino acid analyzer (Hitachi 835, Ibaragi, Japan). Age-adjusted IHD mortality rates in the relevant populations were calculated using the direct standard method. The results indicated that (a) percentiles 25%, 50% and 75% of the distributions of 24-h taurine excretion showed large variations in the study populations. Median values of taurine ranged from 191.6 μmol/day (St John, Canada) to 2,180.6 μmol/day (Beppu, Japan) in males, and from 127.5 μmol/day (Moscow, Russia) to 1,590.0 μmol/day (Beppu, Japan) in females. The highest overall median value of taurine was found in the Japanese population samples, followed by the Chinese samples (Shanghai and Taiwan). European, North American and oceanic Caucasians, however, had much lower median values of taurine, except in the cases of the samples from France and Spain. (b) Median values of taurine were significantly associated negatively with age-adjusted IHD mortality rates across the 24 study population samples in men (R2=0.42, p<0.01), and in women (R2=0.55, p<0.01). These negative associations remained significant after adjustment for serum total cholesterol, body mass index and urinary sodium to potassium ratios. In conclusion, the study provides, for the first time, a cross-sectional database on distribution of 24-h urinary taurine excretion in 24 population samples worldwide. A strong and inverse association between population levels of taurine excretion and IHD mortality was observed. (Hypertens Res 2001; 24: 453-457)

著者

Masataka IWANE Mikio ARITA Shigehiro TOMIMOTO Osamu SATANI Masanobu MATSUMOTO Kazuhisa MIYASHITA Ichiro NISHIO

出版者

The Japanese Society of Hypertension

雑誌

Hypertension Research (ISSN:09169636)

巻号頁・発行日

vol.23, no.6, pp.573-580, 2000 (Released:2006-08-10)

参考文献数

30

被引用文献数

103 136

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We investigated the effects of walking 10, 000 steps/day or more on blood pressure and cardiac autonomic nerve activity in mild essential hypertensive patients. All subjects were males aged 47.0±1.0 (mean±SEM) years old. The original cohort consisted of 730 people in a manufacturing industry who measured the number of steps they walked each day using a pedometer. Eighty-three of these subjects walked 10, 000 steps/day or more for 12 weeks. Thirty-two of these were hypertensives with systolic blood pressure (SBP) greater than 140mmHg and/or diastolic blood pressure (DBP) greater than 90mmHg. Thirty of these hypertensive subjects (HT) were examined twice, once during the pre- and once during the post-study period, for body mass index (BMI), maximal oxygen intake (VO2max), blood pressure, heart rate (HR), and autonomic nerve activity by power spectral analysis of SBP and HR variability. In the HT group, walking 13, 510±837 steps/day for 12 weeks lowered blood pressure (from 149.3±2.7/98.5±1.4 to 139.1±2.9/90.1± 1.9mmHg; p<0.01, respectively). In both the 34 normotensive controls and 17 hypertensive sedentary controls, blood pressure did not change. Walking also significantly lowered low-frequency fluctuations in SBP as an index of sympathetic nerve activity, from 1.324±0.192 to 0.738±0.154 mmHg2/Hz (p<0.05). VO2max rose significantly from 26.1±2.4 to 29.5±2.5ml/kg/min (p<0.05). There were no changes in parasympathetic nerve activity, baroreceptor reflex sensitivity, or BMI. Our results indicate that walking 10, 000 steps/days or more, irrespective of exercise intensity or duration, is effective in lowering blood pressure, increasing exercise capacity, and reducing sympathetic nerve activity in hypertensive patients. (Hypertens Res 2000; 23: 573-580)

著者

Sei TSUNODA Yuhei KAWANO Takeshi HORIO Naoki OKUDA Shuichi TAKISHITA

出版者

The Japanese Society of Hypertension

雑誌

Hypertension Research (ISSN:09169636)

巻号頁・発行日

vol.25, no.2, pp.167-173, 2002 (Released:2002-09-13)

参考文献数

32

被引用文献数

59 71

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Cross-sectional studies have shown that home blood pressure (BP) correlates with hypertensive target organ damage better than clinic BP. However, there have been few longitudinal studies regarding the predictive value of home BP on the changes in organ damage in treated hypertensive patients. Clinic and home BP over a 12-month period, antihypertensive medication use, echocardiographic and electrocardiographic results, and serum creatinine and urinary protein levels were examined in 209 treated hypertensive patients in 1993. These patients were prospectively followed for 5 years. The patients were divided into 4 subgroups according to hypertension control as follows: good control (<140⁄90 mmHg for clinic BP, <135⁄85 mmHg for home BP), improved, worsened, and poor control. The average clinic BP was 147.0±14.9⁄87.0±7.6 mmHg (mean±SD) in 1993 and 146.0±13.7⁄84.1±7.5 mmHg in 1998. The average home BP was 136.8±10.4⁄84.3±7.6 mmHg in 1993 and 136.1±9.7⁄81.2±7.7 mmHg in 1998. The left ventricular mass index (LVMI) positively correlated with both home systolic BP and clinic systolic BP in 1998 but not in 1993. The correlation tended to be closer for home BP than for clinic BP. LVMI did not change in patients with good or improved home systolic BP, while it increased in those with poor or worsened home systolic BP. The relationship between changes in LVMI and clinic BP was not significant. In conclusion, Home BP was more effective than clinic BP as a predictor of changes in left ventricular hypertrophy in treated hypertensive patients. Home BP should be controlled to below 135⁄85mmHg to prevent cardiac hypertrophy.(Hypertens Res 2002; 25: 167-173)

著者

Kazuomi KARIO S. McEWEN Bruce G. PICKERING Thomas

出版者

The Japanese Society of Hypertension

雑誌

Hypertension Research (ISSN:09169636)

巻号頁・発行日

vol.26, no.5, pp.355-367, 2003 (Released:2003-12-10)

参考文献数

109

被引用文献数

104 148

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There is growing evidence that stress contributes to cardiovascular disease. Chronic stress contributes to the atherosclerotic process through increased allostatic load, which is mediated by the neuroendocrine and immune systems (sympathetic nervous system and hypothalamus-pituitary adrenal axis) and related chronic risk factors (insulin resistance syndrome, hypertension, diabetes, and hyperlipidemia). In addition, acute stress can trigger cardiovascular events predominantly through sympathetic nervous activation and potentiation of acute risk factors (blood pressure increase, endothelial cell dysfunction, increased blood viscosity, and platelet and hemostatic activation). Earthquakes provide a good example of naturally occurring acute and chronic stress, and in this review we focus mainly on the effects of the Hanshin-Awaji earthquake on the cardiovascular system. The Hanshin-Awaji earthquake resulted in a 3-fold increase of myocardial infarctions in people living close to the epicenter, particularly in women, with most of the increase occurring in nighttime-onset events. There was also a near doubling in the frequency of strokes. These effects may be mediated by changes in hemostatic factors, as demonstrated by an increase of D-dimer, von Willebrand factor, and tissue-type plasminogen activator (tPA) antigen. Blood pressure also increased after the earthquake, and was prolonged for several weeks in patients with microalbuminuria. (Hypertens Res 2003; 26: 355-367)

著者

Hisashi HARADA Kazuhisa KITAZAKI Takeshi TSUJINO Yasuhiro WATARI Sachiyo IWATA Hidemi NONAKA Takeshi HAYASHI Tatsuya TAKESHITA Kanehisa MORIMOTO Mitsuhiro YOKOYAMA

出版者

The Japanese Society of Hypertension

雑誌

Hypertension Research (ISSN:09169636)

巻号頁・発行日

vol.23, no.3, pp.277-284, 2000 (Released:2006-08-10)

参考文献数

34

被引用文献数

20 26

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Taurine is known to lower blood pressure in essential hypertension and some experimental hypertensive models. Taurine has also been reported to activate aldehyde dehydrogenase and to inhibit the elevation of plasma acetaldehyde concentration after ethanol intake. Because acetaldehyde, the first metabolite of ethanol, is suspected to be responsible for many adverse effects of alcohol consumption, we examined the effect of taurine supplementation on ethanol-induced hypertension and abnormalities in the intracellular cation metabolism in Witar-Kyoto rats. In Study 1, systolic blood pressure and intraplatelet free calcium were significantly higher in rats who received 15% ethanol in drinking water than in control rats. Oral taurine supplementation (1% taurine and 15% ethanol in drinking water) completely prevented the development of ethanol-induced hypertension. Intraerythrocyte sodium and intraplatelet free calcium were significantly decreased in taurine-supplemented rats as compared with rats who received 15% ethanol only. In Study 2, hemoglobin-associated acetaldehyde (HbAA) was measured as a marker of protein-bound acetaldehyde. HbAA was significantly elevated in rats who received 5% ethanol in drinking water as compared with control rats. Taurine supplementation (1% taurine and 5% ethanol in drinking water) significantly decreased HbAA. Our findings suggest that the oral supplementation of taurine prevents ethanol-induced hypertension by decreasing protein bound acetaldehyde and altering the cation handling by the membrane. (Hypertens Res 2000; 23: 277-284)

著者

Masanori IWASE Kojiro ICHIKAWA Kenji TASHIRO Kenzo IINO Noriyasu SHINOHARA Setsuro IBAYASHI Mototaka YOSHINARI Masatoshi FUJISHIMA

出版者

The Japanese Society of Hypertension

雑誌

Hypertension Research (ISSN:09169636)

巻号頁・発行日

vol.23, no.5, pp.503-510, 2000 (Released:2006-08-10)

参考文献数

40

被引用文献数

18 18

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We compared the effects of hypothalamic obesity induced by neonatal monosodium glutamate (MSG) treatment between spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Newborn WKY and SHR were injected intraperitoneally with 4mg/kg body weight of MSG daily for 5 days. At 6 months of age, the obesity of SHR was more advanced than that of WKY, but at 14 months of age the severity of obesity was similar between the two strains. Hypertriglyceridemia was enhanced in MSG-treated SHR as compared with MSG-treated WKY. Systolic blood pressure measured by the tail-cuff method was consistently lower in MSG-treated SHR than in control SHR, whereas blood pressure was not affected by neonatal MSG treatment in WKY. Food restriction reduced body weight more in control SHR than in control WKY, with the former also showing enhanced ketogenesis. Neonatal MSG treatment abolished the accelerated reduction of body weight in SHR. Serum leptin concentration was markedly increased in MSG-treated obese rats, though no differences were seen between WKY and SHR in the control or MSG-treated groups. Serum leptin was closely correlated with both Lee obese index and mesenteric fat weight over the strain. Blood flow in interscapular brown adipose tissue (BAT) measured by Laser Doppler flowmetry was significantly increased in response to β3-adrenoceptor agonist BRL26830A in both the control and MSG-treated rats. However, the response of blood flow was not affected by MSG treatment or strain difference. The present study demonstrated some strain differences in response to neonatal MSG treatment between WKY and SHR. These differences could not be explained by the difference in serum leptin level or β3-adrenergic reactivity in BAT. (Hypertens Res 2000; 23: 503-510)

著者

Kazue ITOH Katsumi IMAI Takashi MASUDA Shimako ABE Misuzu TANAKA Ririko KOGA Hitomi ITOH Toshitaka MATSUYAMA Motoomi NAKAMURA

出版者

The Japanese Society of Hypertension

雑誌

Hypertension Research (ISSN:09169636)

巻号頁・発行日

vol.25, no.6, pp.881-886, 2002 (Released:2003-06-30)

参考文献数

30

被引用文献数

31 44

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Insulin resistance is thought to raise blood pressure. Recently, a significant positive relationship between mean blood pressure and plasma leptin levels, but there have been no reports dealing with the relationship between blood pressure and either insulin resistance or serum leptin levels after weight loss. In the present work, we attempted to clarify the relationship between changes in blood pressure and either the serum leptin level or the insulin level in 102 moderately obese females (mean body mass index (BMI), 29.5±0.5 kg/m2; age, 47.0±0.9) during a 3 month period. No differences in age, fat-mass, homeostasis model assessment (HOMA), the summation of insulin (ΣIRI), plasma renin activity (PRA) or 24 h norepinephrine excretion (24hU-NE) were observed between the hypertensive (HT) group (n =31) and normotensive (NT) group (n =71) before weight loss, but the basal serum leptin was significantly higher in the HT (16.8±1.1 ng/ml) than in the NT group (15.2±0.8 ng/ml), after adjusting for abdominal total fat. After a 3 month weight reduction program, the total abdominal fat, serum leptin and ΣIRI significantly decreased in both groups. The systolic blood pressure (SBP)/diastolic blood pressure (DBP) significantly decreased from 144/84 to 130/77 mmHg only in the HT but not in the NT group. The PRA decreased in both groups, while the 24hU-NE significantly decreased only in the HT group. The changes in the leptin level were significantly correlated with the changes in both ΣIRI and HOMA after weight loss in the two groups, respectively. Finally, a statistically significant positive correlation was observed between the changes in the leptin and the changes in the mean blood pressure (MBP) (r =0.412, p <0.05) only in the HT group. Multiple regression analysis revealed that the changes in MBP were independently associated with the changes in 24hU-NE and the changes in either ΣIRI or HOMA in all subjects. However, a statistically significant positive correlation was observed between the changes in MBP and the changes in leptin levels even after adjusting for the total abdominal fat, 24hU-NE and either ΣIRI or HOMA (both expressed as a percentage of the baseline value) in a multiple regression analysis only in the HT group. These results suggest that leptin may play a role in the pathophysiology of obese hypertension. (Hypertens Res 2002; 25: 881-886)

著者

Aya MARUYAMA Tomohiro NAKAYAMA Naoyuki SATO Yoshihiro MIZUTANI Kiyohide FURUYA Tatsuo YAMAMOTO

出版者

The Japanese Society of Hypertension

雑誌

Hypertension Research (ISSN:09169636)

巻号頁・発行日

vol.27, no.12, pp.903-909, 2004 (Released:2005-05-16)

参考文献数

25

被引用文献数

26 26

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The pathophysiology of preeclampsia (PE) remains uncertain despite many research efforts. Actual hypotheses seek to explain the vascular damage that characterizes the disease. Recently, it was reported that the mouse disrupted estrogen receptor β (ESR2) gene was associated with abnormal vascular function and hypertension. Moreover, some investigators have reported that subjects with a family history of hypertension have a statistically significant increased risk for PE. Thus, it is thought that the pathophysiology of PE overlaps that for hypertension. The aim of the present study was to investigate the relationships between single nucleotide polymorphisms (SNPs) in the human ESR2 gene and PE in Japanese subjects, and to assess the involvement of a family history of hypertension in these relationships. Based on a database search on the web site of the National Center of Biotechnology Information (NCBI), we chose four SNPs in the human ESR2 gene, and performed an association study in 84 PE patients and 160 age-matched non-PE subjects. The overall distribution in each SNP did not differ significantly between the two groups. However, after dividing the groups into subjects with and without a family history of hypertension, the allelic distribution of one of the SNPs (rs928554) revealed a positive association. Thus, a possible mutation linked to a SNP may prescribe a genetic predisposition for patients with a family history of hypertension in PE. (Hypertens Res 2004; 27: 903-909)

著者

Kan SAITO Nobukazu ISHIZAKA Toru AIZAWA Masataka SATA Naoyuki ISO-O Eisei NOIRI Minoru OHNO Ryozo NAGAI

出版者

The Japanese Society of Hypertension

雑誌

Hypertension Research (ISSN:09169636)

巻号頁・発行日

vol.27, no.8, pp.599-607, 2004 (Released:2004-10-19)

参考文献数

30

被引用文献数

18 27

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We have previously shown that abnormal iron metabolism might be one underlying mechanism of the renal damage observed in the angiotensin II-infused rat. Transforming growth factor-β1 (TGF-β1) is known to play a crucial role in the development of renal damage induced by activation of the renin-angiotensin-aldosterone system. The purpose of the present study was to examine the effects of an iron chelator and a free radical scavenger on the angiotensin II-induced upregulation of TGF-β1 in the kidney. Rats were given angiotensin II (0.7 mg/kg/day) via osmotic minipumps for 7 days. The expressions of the mRNAs of TGF-β1 and collagen types I and IV were significantly increased in response to angiotensin II treatment. Histologic analysis showed that TGF-β1 expression was upregulated mainly in tubular epithelial cells, and occasionally in glomerular and perivascular cells, some of which were identified as monocytes and/or macrophages. Although tubular cells that overexpressed TGF-β1 did not contain iron particles, angiotensin II-induced TGF-β1 upregulation was suppressed by the iron chelator and the free radical scavenger. The free radical scavenger also suppressed angiotensin II-induced upregulation of heme oxygenase-1, an oxidative-stress sensitive gene. By contrast, administration of iron dextran to rats induced upregulation of TGF-β1 mRNA. Collectively, these data suggest that the renal iron overload and presumed subsequent increase in oxidative stress play a role in angiotensin II-induced upregulation of the mRNAs of TGF-β1 and collagen types I and IV in the kidney. (Hypertens Res 2004; 27: 599-607)