Hypertension Research
Online ISSN : 1348-4214
Print ISSN : 0916-9636
ISSN-L : 0916-9636
Volume 22, Issue 3
Displaying 1-10 of 10 articles from this issue
  • Ryuichi Morishita, Atsushi Moriguchi, Jitsuo Higaki, Toshio Ogihara
    1999 Volume 22 Issue 3 Pages 161-167
    Published: 1999
    Released on J-STAGE: August 10, 2006
    JOURNAL FREE ACCESS
    Hepatocyte Growth Factor (HGF) is a mesenchyme-derived pleiotropic factor that regulates cell growth, cell motility, and morphogenesis of various cells, and is thus considered a humoral mediator of epithelial-mesenchymal interactions. We previously identified HGF as a novel member of the family of endothelium-specific growth factors. Moreover, the presence of a local HGF system (HGF and its specific receptor, c-met) has been demonstrated in vascular cells both in vitro and in vivo. HGF might contribute to the protection and/or repair of vascular endothelial cells injured by high blood pressure. If so, serum HGF level might be elevated in response to endothelial cell damage. To test this hypothesis, we measured serum levels of HGF in hypertensive and normotensive patients. Serum HGF concentration in hypertensive patients without any complications was significantly higher than that in normal subjects. Interestingly, serum HGF concentration in hypertensive patients with complications was significantly higher than that in either hypertensive patients without complications or normotensive subjects. Of importance, hypertensive patients treated with antihypertensive drugs showed the same level of serum HGF concentration as normotensive subjects. In contrast, serum HGF concentration in diabetic patients without hypertension was significantly lower than that in normal subjects, whereas serum HGF concentration in diabetic patients with hypertension was significantly higher than that in normal subjects. Moreover, serum HGF concentration in diabetic patients with hypertensive complications was even higher than that in diabetics without complications. This review discusses the possibility that HGF may be considered as a new index of the severity of hypertension. (Hypertens Res 1999; 22: 161-167)
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  • Hiroshi Kawabe, Hirotaka Shibata, Hiroshi Hirose, Minako Tsujioka, Iku ...
    1999 Volume 22 Issue 3 Pages 169-172
    Published: 1999
    Released on J-STAGE: August 10, 2006
    JOURNAL FREE ACCESS
    This study was designed to examine the relationships between birth weight or current body weight and blood pressure (BP) or cholesterol in 178 Japanese high school students (98 male, 80 female, age 15-16 yr). All subjects were born after a full-term pregnancy (gestational age ≥38wk) with a birth weight ≥2, 500g; these data were obtained from routine obstetrical records. At a health check-up, nurses used an automatic device to perform two consecutive BP measurements with each subject in a sitting position after resting for at least 5min. Serum total and high-density lipoprotein (HDL) cholesterol levels were measured. Birth weight was not related to BP, but was inversely related to serum total cholesterol in both males (r=-0.241, p<0.05) and females (r=-0.351, p<0.01). Current body weight was significantly related to systolic BP (r=0.369, p<0.01), diastolic BP (r=0.216, p<0.05), and HDL cholesterol level (r=-0.224, p<0.05) in males, but not in females. Although no relationship was demonstrated between birth weight and BP level in young Japanese students without intrauterine growth retardation, an inverse relationship between birth weight and serum total cholesterol level was found. There was a gender difference in the relationship between current body weight and either BP or HDL cholesterol in these subjects. (Hypertens Res 1999; 22: 169-172)
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  • Minori Higashiyama, San-e Ishikawa, Takako Saito, Tomoatsu Nakamura, I ...
    1999 Volume 22 Issue 3 Pages 173-180
    Published: 1999
    Released on J-STAGE: August 10, 2006
    JOURNAL FREE ACCESS
    The present study was undertaken to determine whether transforming growth factor (TGF)-β1 modulates the cellular actions of arginine vasopressin (AVP) in cultured rat glomerular mesangial cells. AVP increased cytosolic free calcium ([Ca2+]i), and TGF-β1 dose-dependently reduced the AVP-mobilized [Ca2+]i. Such an inhibition by exogenous TGF-β1 was abolished by liposomal transfection of antisense oligodeoxynucleotide for the TGF-β type II receptor. AVP activated mitogen-activated protein (MAP) kinase, which was significantly reduced by 1ng/ml TGF-β1. AVP increased [3H] thymidine incorporation into mesangial cells in a dose-dependent manner, and 1ng/ml TGF-β1 significantly reduced the AVP-stimulated [3H] thymidine incorporation. However, 10μM antisense oligodeoxynucleotide for the TGF-β type II receptor seemed to attenuate the inhibition by TGF-β1. 1×10-7M AVP significantly increased inositol 1, 4, 5-trisphosphate (IP3) production by 1.8-fold, but this production was totally blunted by 1ng/ml TGF-β1. TGF-β1 did not affect [3H] AVP receptor binding. 1×10-6M AVP concentration stimulated TGF-β1 production in mesangial cells by 4-fold. These results indicate that TGF-β1 inhibits the cellular signaling of AVP at steps beyond the AVP receptors and prior to the phospholipase C activation, and that TGF-β1 may participate in a negative feedback regulation on the cellular action of AVP in glomerular mesangial cells. (Hypertens Res 1999; 22: 173-180)
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  • Koji Fujii, Susumu Ohmori, Uran Onaka, Isao Abe, Masatoshi Fujishima
    1999 Volume 22 Issue 3 Pages 181-186
    Published: 1999
    Released on J-STAGE: August 10, 2006
    JOURNAL FREE ACCESS
    Although salt intake and blood pressure are correlated, with hypertensives tending to exhibit higher blood pressure sensitivity to salt than normotensives, the precise mechanisms underlying this relationship remain unclear. This study aimed to determine whether salt-loading affects arterial membrane properties of spontaneously hypertensive rats (SHR). SHR and age-matched Wistar Kyoto rats (WKY) received either an 8% high salt diet or standard rat chow from 6 to 16wk of age. Systolic blood pressure was significantly higher in salt-loaded SHR than in control SHR (267±7 vs. 235±5mmHg, p< 0.05). The membrane potential of isolated conduit and resistance arteries of the superior mesenteric vascular bed, measured with microelectrodes, was less negative in salt-loaded SHR than in control SHR or salt-loaded WKY (conduit arteries, -39.9±0.3 vs. -44.5±0.4 or -47.4±0.4mV, respectively, p <0.05 for each; resistance arteries, -55.5±0.5 vs. -62.5±0.5 or -67.0±0.5mV, respectively, p< 0.05 for each). Furthermore, conduit arteries of salt-loaded SHR exhibited spontaneous electrical activity (4-13mV, 1-3/min), which was sensitive to ONO-3708, a thromboxane A2/prostaglandin H2 receptor ntagonist. These findings suggest that salt-loading in SHR leads to a membrane depolarization in both conduit and resistance arteries, as well as to spontaneous electrical activity, presumably mediated by eicosanoids, in conduit arteries. These alterations in membrane properties might contribute to the exacerbation of hypertension and/or the target organ damage after salt loading in SHR. (Hypertens Res 1999; 22: 181-186)
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  • Yutaka Kitami, Motofumi Maguchi, Wataru Nishida, Takafumi Okura, Katsu ...
    1999 Volume 22 Issue 3 Pages 187-193
    Published: 1999
    Released on J-STAGE: August 10, 2006
    JOURNAL FREE ACCESS
    Calponin has been implicated in the regulation of smooth muscle contraction. Basic calponin, one of the calponin isoforms, is expressed exclusively in smooth muscle cell (SMC)-rich tissues, and is considered to be a phenotypic marker of differentiated SMC. To define the molecular mechanism of SMC-specific gene transcription in humans, we isolated and characterized the 5′-flanking region of this gene. Sequence analysis revealed that several putative cis-acting elements were clustered within a 500-bp sequence upstream of the transcription start site. However, the 1.9-kb promoter region obtained herein lacked a completely matched consensus sequence of the CArG box that is commonly identified in the promoter region of other SMC-specific genes. A luciferase assay demonstrated that the 1.9-kb promoter region was sufficient to drive a basal transcriptional activity not only in human vascular smooth muscle cells (VSMC) but also in HeLa cells. In particular, the sequence between positions -1, 906 and -867 had a significantly higher transcriptional activity in VSMC than in HeLa cells. In contrast, the promoter activity was drastically decreased between positions -327 and -257 in both types of cells. These results indicate that the sequence spanning from position -327 to -257 contains an essential domain involved in the basal transcriptional activity of the human basic calponin gene, and that the distal region of the 1.9-kb 5′-flanking sequence presented herein may play a pivotal role in the phenotypic modulation of VSMC. (Hypertens Res 1999; 22: 187-193)
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  • Takao Saruta, Kikuo Arakawa, Osamu Iimura, Keishi Abe, Hiroaki Matsuok ...
    1999 Volume 22 Issue 3 Pages 197-202
    Published: 1999
    Released on J-STAGE: August 10, 2006
    JOURNAL FREE ACCESS
    To compare the incidence of cough between two angiotensin converting enzyme (ACE) inhibitors, imidapril and enalapril, comparative crossover study was performed in 489 patients (228 men and 261 females) with essential or renal parenchymal hypertension. Patients were randomly assigned to one of two treatment groups, a group receiving imidapril for 12wk (Period I) followed by enalapril for 12wk (Period II), and a group in which the order of drugs was reversed. The occurrence of cough during treatment was monitored by questionnaire in all cases. There were no differences in background characteristics between the two groups. The incidence of cough during Period I was 15.2% (32/210) in the group initially treated with imidapril (Group IE) and 38.6% (85/220) in the group initially treated with enalapril (Group EI), the difference being statistically significant (p<0.001). During Period I, decrease in blood pressure was observed in 63.9% (115/180) of Group IE and 64.6% (115/178) of Group EI patients. In approximately half of the patients in Group EI who developed cough during Period I and in whom the treatment was subsequently switched to imidapril, cough subsequently disappeared. It was concluded that the incidence of cough was significantly less under imidapril than under enalapril treatment, while there was no difference in the antihypertensive effects of the two ACE inhibitors. (Hypertens Res 1999; 22: 197-202)
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  • Yinong Jiang, Katsuhiko Kohara, Kunio Hiwada
    1999 Volume 22 Issue 3 Pages 203-207
    Published: 1999
    Released on J-STAGE: August 10, 2006
    JOURNAL FREE ACCESS
    Numerous in vitro studies have indicated that low shear stress may contribute to intimal thickening and development of atherosclerosis. In the present study, we investigated wall shear stress in hypertensive patients and its relevance to atherosclerosis in the carotid arteries by means of a non-invasive technique. Fifty-five hypertensive patients and 23 normotensive controls were investigated. Intima-media thickness, number of plaques, internal dimension and blood flow velocity of the carotid artery were evaluated. Wall shear stress was calculated using the Poiseuillean parabolic model of velocity distribution as follows: shear stress=4×blood viscosity×central line flow velocity/internal dimension. Hypertensive patients showed increased intima-media thickness and dilated common carotid arterial dimension relative to normotensive controls. There was no difference in blood viscosity between the two groups. Both the mean shear stress and systolic peak shear stress were significantly lower in hypertensive patients than normotensive controls. Further, wall shear stress at both mean and peak velocity was significantly and negatively related to intima-media thickness and number of plaques in hypertensive patients, as well as in the total study population. These findings indicate that structural and functional alterations in the common carotid artery of hypertensive patients further precipitates atherosclerosis through low shear stress. (Hypertens Res 1999; 22: 203-207)
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  • Ming Gao, Katsumi Ikeda, Hiroyuki Hattori, Ayako Miura, Yasuo Nara, Yu ...
    1999 Volume 22 Issue 3 Pages 209-215
    Published: 1999
    Released on J-STAGE: August 10, 2006
    JOURNAL FREE ACCESS
    In this assessment of cardiovascular risk factors, we examined the association between dietary habits and blood pressure (BP) according to the World Health Organization (WHO) CARDIAC Study protocols in three Chinese populations aged 47-57 in Guangzhou prefecture (GZ group; 141 males, 158 females), Guiyang prefecture (GY group; 101 males, 103 females) and Taiwan (TW group; 102 males, 98 females). The same survey was repeated 10 yr later in the GY group to follow-up the past trends (MONALISA study). The observed systolic BP (SBP), diastolic BP (DBP), and body mass index (BMI), as well as the rates of hypertension, obesity and antihypertensive medication use were significantly higher in both genders in the TW group compared to the groups GZ and GY. There was no significant difference in SBP or DBP in either gender between groups GZ and GY. Blood analyses revealed that the levels of serum total cholesterol (T-CHO), and HbA1c, and the rates of hypercholesterolemia and high HbA1c were significantly higher in both genders in the TW than in the GZ and GY groups. No significant difference among the populations was observed in 24-h urinary sodium or magnesium excretion in either gender. In the combined total populations of men and women, however, significant positive correlations were observed between BMI and each of SBP, DBP, T-CHO, and glycohemoglobin in both genders. A food frequency analysis revealed significantly greater meat consumption and significantly less tea consumption and vegetable intake in the TW than in the GY and GZ groups. Both SBP and DBP have increased significantly over the past 10 yr in the GY group in both genders, and T-CHO as well as the rate of hypercholesterolemia increased over the same period in both genders. In conclusion, cardiovascular risk factors leading to hypertension, such as obesity, hypercholesterolemia and diabetes mellitus, are emerging in urbanized Taiwan and developing Guiyang due to the loss of traditional dietary habits. (Hypertens Res 1999; 22: 209-215)
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  • Aimin Dang, Deyu Zheng, Bing Wang, Yuqing Zhang, Penghua Zhang, Minfu ...
    1999 Volume 22 Issue 3 Pages 217-221
    Published: 1999
    Released on J-STAGE: August 10, 2006
    JOURNAL FREE ACCESS
    To elucidate the relationship between the development of left ventricular hypertrophy (LVH) in hypertension and the development of both the cardiac sympathetic nervous and renin-angiotensin systems, as measured by norepinephrine and angiotensin II levels, respectively. In this longitudinal study, we compared blood pressure (BP), left ventricular weight, and norepinphrine (NE) and angiotensin II (Ang II) concentrations, in Spontaneously Hypertensive Rats (SHR) and age-matched Wistar-Kyoto (WKY) rats at 5, 10, 15, 20, and 28 wk of age. Blood pressure, plasma and ventricular Ang II and tissue NE were measured by the tail-cuff method, radioimmunoassay, and high-performance liquid chromatography (HPLC), respectively. At 5 wk, systolic blood pressure was the same in both strains. But the left ventricular plus septum weight to body weight (LVSW/BW) ratio was higher in SHR than in WKY rats (p <0.01), which finding may have been related to the increased cardiac tissue NE concentration, and this increase tended to parallel the rise in blood pressure. Both left ventricle and forelimb muscle NE concentrations were significantly higher in SHR than in WKY rats at 5, 10, and 15 wk of age (p<0.01, respectively), and were similar at 20 and 28 wk of age. The heart and plasma Ang II levels decreased with age, which results were in keeping with the known developmental tendencies of the biological aging progress. There was no significant difference in plasma Ang II levels between the two strains from 5 to 20 wk, whereas these levels were remarkably higher in WKY than in SHR rats at 28 wk (p<0.01). Otherwise, the left ventricular tissue Ang II concentrations were significantly higher in SHR than in WKY rats at the late stage (from 15 to 28 wk), which may have contributed to the late-stage cardiac hypertrophy. These results suggested that the sympathetic nervous system (SNS) and the renin-angiotensin-system (RAS) in SHR may contribute to the pathogenesis of hypertension and LVH at the early and late stages, respectively. (Hypertens Res 1999; 22: 217-221)
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  • Jing Zi Li, Chun Hua Zhou, Ling Yu, Hai Yan Wang
    1999 Volume 22 Issue 3 Pages 223-228
    Published: 1999
    Released on J-STAGE: August 10, 2006
    JOURNAL FREE ACCESS
    It has been well demonstrated that angiotensin-converting enzyme inhibitors (ACEIs) can retard the progression of renal failure and kidney sclerosis in patients and animal models with glomerular diseases. The aim of this study was to observe the influences of ACEI on intrarenal Ang II and TGFβ1 local formation and their relation to renal protective effects. Experimental glomerulosclerosis with nephrotic syndrome was induced in unilateral nephrectomized rats with repeated injections of adriamycin. Rats were randomly divided into three groups: 1) a sham-operated control group (n=8); 2) an NS group treated with ACEI (benazepril 4mg/kg/d) (n=10), and 3) an NS group not treated (n=10). After 8 wk, serum, urine and renal tissue were collected for study. ACE activity and Ang II concentration in renal tissue were measured by colorimetry and radioimmunoassay, respectively. Immunohistochemistry staining was employed for transforming growth factor-β1 (TGFβ1) and extracellular matrix (ECM) examination. TGFβ1 mRNA was assessed by in situ hybridization. Compared with those of non-treated nephropathy rats, ACE activity (13.39±5.02 vs. 49.13±12.92U/ml, p<0.01) and Ang II (402.61±80.22 vs. 751.63±137.45pg/mg/pr p<0.01) in renal tissue were significantly inhibited in the rats treated with ACEI. At the same time, proteinuria was significantly reduced (155.06±103.56 vs. 421.11±148.45 mg/24h, p<0.01) and renal function improved (Scr 76.3±33.1 vs. 107.1±71.0, p<0.05), concomitant with a reduction in the glomerular sclerosis index (30.6±19.5 vs. 120.3±61.9, p<0.01) and a reduction in ECM accumulation such as Col IV, III, LN and FN (29.2±9.8 vs. 76.8±12.4; 29.5±12.4 vs. 85.9±11.5; 26.0±5.1 vs. 69.6±1.73; 32.4±12.4 vs. 70.5±13.5; p<0.01 in all cases). In the ACEI treated group, these histologic benefits coincided with a reduced expression of TGFβ1 in both tubular cells and sclerosed glomeruli in protein as well as mRNA level. These findings provide further evidence that ACEI (benazepril) can prevent the progression of renal damage in both the function and morphologic changes which associated with a down-regulation of intrarenal Ang II level through the relative inhibition of renal ACE activity. The blocking of the Intrarenal renin angiotensin system (RAS) might contribute to the inhibition of TGFβ1 local formation and the TGFβ1-mediated ECM accumulation that are related to the renal protective effects of ACEI. (Hypertens Res 1999; 22: 223-228)
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