Hypertension Research
Online ISSN : 1348-4214
Print ISSN : 0916-9636
ISSN-L : 0916-9636
Volume 24 , Issue 4
July
Showing 1-19 articles out of 19 articles from the selected issue
Original Articles
Clinical studies
  • Akiyo TANABE, Mitsuhide NARUSE, Tetsuya OGAWA, Fumio ITO, Sachiko TAKA ...
    2001 Volume 24 Issue 4 Pages 331-336
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    We compared dynamic computer tomographic CT images of 3 cases of juxtaglomerular (JG) cell tumor with those of 8 cases of renal cell carcinoma (RCC). The JG cell tumor was visualized as a low- to high-density area in case 1, a low-density area in case 2, and a low- to iso-density area in case 3 before contrast enhancement. None of the JG cell tumors were stained during the early phase (1 min), but all were stained moderately during the late phase (5 min) after contrast enhancement. Although all cases of RCC were visualized as a low- to iso-density area before contrast enhancement, they were intensely stained during the early phase with significant washout during the late phase. The present results suggest that the dynamic CT scan is useful in the differential diagnosis of the JG cell tumor and RCC. (Hypertene Res 2001; 24: 331-336)
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  • Masazumi AKAHOSHI, Yasuko AMASAKI, Midori SODA, Tan TOMINAGA, Shinichi ...
    2001 Volume 24 Issue 4 Pages 337-343
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    The relation between fatty liver, detected by ultrasonography as a marker of visceral fat accumulation, and coronary risk factors was studied in 810 elderly men and 1,273 elderly women in Nagasaki, Japan from 1990 to 1992. The prevalence of fatty liver was 3.3% in the male and 3.8% in the female non-obese participants (BMI, body mass index<26.0 kg/m2) and 21.6% in the male and 18.8% in the female obese participants (26.0 kg/m2≤BMI). Fatty liver was significantly (p< 0.01) related to hypercholesterolemia and hypertriglyceridemia in the men and to hypertension, hypercholesterolemia, low-HDL cholesterol, hypertriglyceridemia and diabetes mellitus or impaired glucose tolerance (DM+IGT) in the women independent of age, obesity, smoking and drinking. Non-obesity with fatty liver, rather than obesity with or without fatty liver, had the highest odds ratio for hypertension and low-HDL cholesterol in the men and for hypercholesterolemia, low-HDL cholesterol, hypertriglyceridemia and DM+IGT in the women. The prevalence of fatty liver is the same in elderly men and women, and fatty liver is an independent correlate of coronary risk factors in the elderly. (Hypertene Res 2001; 24: 337-343)
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  • Shinichiro FUJISHIMA, Yusuke OHYA, Hiroshi SUGIMORI, Jiro KITAYAMA, Sh ...
    2001 Volume 24 Issue 4 Pages 345-351
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    To appraise the value of transcranial Doppler sonography (TCD) for assessment of hypertensive cerebrovascular damage, the relationship between ambulatory blood pressure (BP) and indices of cerebral circulation determined by TCD was investigated. Subjects were 55 inpatients with or without hypertension, including 13 patients with histories of cerebrovascular attacks. Mean flow velocity (MFV) in the middle cerebral artery was measured by TCD, then the cerebrovascular resistance index (CVRI; mean BP/MFV) and the Fourier PI1 (pulsatility index of the first Fourier harmonic of the flow-velocity waveform) were determined as indices of cerebrovascular resistance. CO2 reactivity of MFV was estimated as an index of cerebrovascular flow reserve. CVRI positively correlated with both daytime and nighttime BP as well as with age (p<0.01). Fourier PI1 positively correlated with nighttime BP and age (p<0.01). CO2 reactivity did not correlate with any of the ambulatory BP parameters, but negatively correlated with age (p<0.01). LV mass index significantly correlated with ambulatory BP parameters, CVRI, and Fourier PI1, but did not correlate with CO2 reactivity. Multiple regression analyses showed that nighttime systolic BP was a significant correlate for CVRI and Fourier PI1, but not for CO2 reactivity, and that history of cerebrovascular attack was significant for CVRI and CO2 reactivity. We conclude that cerebrovascular resistance determined by TCD accords with the results of ambulatory BP and LVMI, and thus could be successfully used to detect the early stage of hypertensive cerebrovascular change. Cerebrovascular flow reserve would be relatively preserved in hypertensive patients without cerebrovascular diseases. (Hypertens Res 2001; 24: 345-351)
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  • Osamu TOCHIKUBO, Junko WATANABE, Kouichi HANADA, Eiji MIYAJIMA, Kazuo ...
    2001 Volume 24 Issue 4 Pages 353-357
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    Accurate measurement of blood pressure (BP) is essential in the diagnosis and treatment of hypertension, but neither auscultatory nor oscillometric methods measure intra-arterial BP accurately in all circumstances. Algorithms for automatic BP-measuring devices differ from manufacturer to manufacturer, and no clear authorized algorithm criteria have yet been established. We have devised a double-cuff sphygmotonometer to measure BP on the basis of clear algorithms, and investigated the accuracy of this new method by comparing it with the photo-oscillometric method, which is the most accurate method for non-invasive measurement of intra-arterial BP. In the new method, a small cuff (3×6 cm) replaces the photo-sensor in the brachial cuff (13×24 cm) of the photo-oscillometric device, and BP is determined by means of the oscillation within the small cuff. The comparison based on procedures of AAMI-protocol was performed in 136 hypertensive patients and 54 normotensive subjects. The difference in systolic BP between the photo-oscillometric and double-cuff methods was −2.26±2.31 mmHg (89% under 5 mmHg), and the corresponding difference in diastolic BP was 1.9±2.50 mmHg (94% under 5 mmHg). In conclusion, we have devised a new double-cuff method which improves on the photo-oscillometric method, and although it seems to be less accurate than the photo-oscillometric method, the clarity of its algorithm makes it superior to the conventional oscillometric and auscultatory methods employing only one cuff. (Hypertens Res 2001; 24: 353-357)
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  • Yasukiyo MORI, Hiroaki MATSUBARA, Atsuko NOSE, Yasunobu SHIBASAKI, Hir ...
    2001 Volume 24 Issue 4 Pages 359-363
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    Hypertension accelerates the progression of renal disease in patients with chronic renal failure. Doxazosin, an α1-antagonist, is an antihypertensive agent with a long half-life. In this study, 15 patients with chronic renal failure were treated only with doxazosin and diuretics for 6 months and their blood pressure, renal parameters and lipid profile were measured. The initial dose of doxazosin was 2 mg/day and it was titrated until blood pressure was normalized. The average dose was 5.6 mg/day. As expected, systolic and diastolic blood pressure were decreased with treatment (165/91 mmHg to 135/73 mmHg). The drop in blood pressure was associated with an increase in glomerular filtration and a decrease in plasma BUN and creatinine levels. Reduction in mean blood pressure and decrease in proteinuria had a significant positive correlation (r=0.048, p=0.007). Proteinuria was decreased from 1.8 mg/day to 1.3 mg/day with doxazosin treatment and triglycerides also decreased, while HDL-cholesterol was increased. No side effects were observed. These results indicate that doxazosin is an efficient depressor agent with renal protective actions and that higher doses of doxazosin can be safely given to patients with chronic renal failure. (Hypertens Res 2001; 24: 359-363)
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  • Shuichi TAKAGI, Shunroku BABA, Naoharu IWAI, Masayuki FUKUDA, Tomohiro ...
    2001 Volume 24 Issue 4 Pages 365-370
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    Excessive alcohol consumption is a potent risk factor for high blood pressure. About half of Japanese show an extremely high sensitivity to alcohol, which is due to a genetic deficiency in an isoenzyme of aldehyde-dehydrogenase with a low Km (ALDH2). It is possible that the effects of alcohol consumption on blood pressure differ according to the ALDH2 genotype. The purpose of the present study was to assess the influence of the ALDH2 genotype on the pressor effects of alcohol. The influence of the ALDH2 genotype on blood pressure was investigated in a large cohort (4, 000 subjects) representing the general population in Japan. The genotype was determined by the TaqMan method. The genotype was significantly associated with alcohol consumption, gamma-GTP level, and HDL cholesterol level in both males and females. The odds ratio for the presence of hypertension for the Glu/Glu genotype in comparison to other genotypes was 1.67 (p<0.0001, odds ratio=1.37−2.08, 95% confidence interval) among males. In contrast, the ALDH2 genotype had no significant effects on blood pressure among females. To investigate whether the ALDH2 genotype affected the sensitivity to the pressor effects of alcohol, we analyzed the effects of the ALDH2 genotype (Lys/Lys+Lys/Glu=0, Glu/Glu=1) and the level of alcohol consumption on blood pressure values after adjusting for age and BMI (residuals after adjusting for age and BMI). Among males, while the level of alcohol consumption significantly affected systolic, diastolic and pulse pressure, no significant interaction was observed between the ALDH2 genotype and the level of alcohol consumption in determining blood pressure levels. These results suggest that the Glu/Glu genotype is a potent risk factor for hypertension among males mainly through its association with the level of alcohol consumption, and that the ALDH2 genotype does not affect the sensitivity to the pressor effects of alcohol. (Hypertens Res 2001; 24: 365-370)
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  • Kazuko MASUO, Hiroshi MIKAMI, Toshio OGIHARA, Michael L. TUCK
    2001 Volume 24 Issue 4 Pages 371-376
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    This study was conducted to clarify the mechanisms involved in the sensitivity for blood pressure (BP) reduction in response to weight loss. In particular, we focused on the contributions of sympathetic nervous system activity and fasting plasma leptin and insulin levels to BP levels during weight loss in obese subjects with weight loss-sensitive and -resistant BP reduction. Sixty-one young, obese untreated hypertensive men (HT) and 52 obese normotensive men (NT) were enrolled in a weight loss program consisting of a low caloric diet and aerobic exercise over a 24-week period. At entry and at week 24, body mass index (BMI), BP, plasma norepinephrine (NE), leptin and insulin were measured. Successful weight loss and BP reduction were respectively defined as a more than a 10% reduction in BMI or mean BP from baseline at week 24. More than 60% of subjects in either group successfully achieved weight loss by this definition. The percentage of subjects who successfully achieved BP reduction was higher (64%) among those subjects who achieved weight loss than among those who did not (22%). Plasma NE level at entry in subjects who failed to achieve BP reduction despite weight loss was significantly higher than that in subjects who succeeded in BP reduction. Plasma leptin and insulin levels were similar between subjects with and without BP reduction. In addition, the absolute decrement and percent decrement in plasma NE in subjects who succeeded in BP reduction were significantly greater than those in subjects who failed to reduce their BP. Absolute and percent decrements in plasma leptin and insulin were similar in both groups. These results suggest that individuals who are resistant to weight loss-induced BP reduction have more sympathetic overactivity both at the outset of and during weight loss. (Hypertens Res 2001; 24: 371-376)
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  • Gregory W. ROSE, Yoshihiko KANNO, Hironori IKEBUKURO, Masaharu KANEKO, ...
    2001 Volume 24 Issue 4 Pages 377-383
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    To investigate the beneficial effects of cilnidipine, a calcium channel blocker that shows high selectivity for N-type receptors, on the progression of chronic renal insufficiency, we compared the efficacy of cilnidipine to that of benazepril, an angiotensin-converting enzyme (ACE) inhibitor with known renal protective effects, in a one-year trial evaluating hypertensive control, serum creatinine, and albuminuria in a cohort of patients. Given the seeming importance of the etiology of chronic renal insufficiency in determining drug efficacy, we limited our study to 20 patients with a single common condition, benign nephrosclerosis. The average age of the patients was 62±4 yaers old. The changes in systolic and diastolic blood pressure over the course of the study year revealed a similar reduction with cilnidipine and benazepril. Both cilnidipine and benazepril induced similar reductions in systolic and diastolic blood pressure over the course of the study year. The baseline levels of serum creatinine were 1.40±0.2 mg/dl and urinary excretion of albumin was 168±10 mg daily. The levels of serum creatinine were not significantly changed throughout the study in either group, although the levels of urinary excretion of albumin were significantly decreased in both groups. There were no significant differences in either of these values between the two groups. In conclusion, both cilnidipine and benazepril equally and effectively reduced blood pressure and albuminuria in hypertensive patients with benign nephrosclerosis in a one-year trial. (Hypertens Res 2001; 24: 377-383)
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Experimental studies
  • Yukio HIROI, Junko HIROI, Sumiyo KUDOH, Yoshio YAZAKI, Ryozo NAGAI, Is ...
    2001 Volume 24 Issue 4 Pages 385-394
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    Increasing evidence has suggested that mitogen-activated protein kinases (MAPKs) play important roles in the development of cardiac hypertrophy. We and others have reported that the activity of MAPKs is tightly regulated by angiotensin II (Ang II) in cardiac myocytes. In the present study, we determined the molecular mechanism of Ang II-induced inactivation of MAPKs in rat neonatal cardiac myocytes. Ang II increased MAPK phosphatase 1 (MKP-1) gene expressions within 10 min. Levels of MKP-1 transcripts peaked at 30 min and gradually decreased thereafter. The increase in MKP-1 mRNA levels was Ang II-concentration dependent. An Ang II type 1 receptor (AT1)-specific antagonist, CV-11974, completely suppressed the Ang II-induced increase in MKP-1 gene expression, while a type 2 receptor (AT2)-specific antagonist, PD-123319, had no significant effects. Induction of MKP-1 gene expressions by Ang II was inhibited by pretreatment with an intracellular Ca2+ chelator, BAPTA-AM, or with the protein kinase C inhibitors, H-7 and Calphostin C. Phorbol ester and Ca2+ ionophore both significantly increased MKP-1 mRNA levels and showed synergistic action. Overexpression of MKP-1 cDNA blocked the Ang II-induced increase in expressions of immediate early response genes. In addition, Ang II-induced MAPK activation was significantly inhibited by pretreatment with CV-11974, but significantly enhanced by pretreatment with PD-123319. Addition of the AT2 agonist, CGP42112A, reduced basal MAPK activities, and pretreatment with PD-123319 abolished MAPK inactivation by CGP42112A. In conclusion, these observations suggest that Ang II negatively regulates MAPKsthrough AT1 receptors by increasing MKP-1 mRNA levels and through AT2 receptors by unknown mechanisms. (Hypertens Res 2001; 24: 385-394)
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  • Shinji MOKUNO, Takayuki ITO, Yasushi NUMAGUCHI, Hideo MATSUI, Yukio TO ...
    2001 Volume 24 Issue 4 Pages 395-401
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    In the current study, we investigated the NO-generation pathway in response to mechanical stimuli in SHR at the prehypertensive stage. To examine the role of NO in coronary autoregulation, we evaluated the effects of L-NAME on the coronary flow in SHR at both the prehypertensive and hypertensive stages. Isolated perfused hearts from 5- and 15-week-old SHR and from age-matched Wistar-Kyoto rats (WKY) were used. After stabilization at 60 mmHg, perfusion pressure was immediately raised to 90 mmHg to record the change in coronary flow for 10 min without (control) or with NO synthesis blockade by Nω-nitro-L-arginine methyl ester (L-NAME). NOx- (nitrite/nitrate) was measured in coronary effluent. At 5 weeks of age, SHR did not have hypertension, while the coronary autoregulation was enhanced. L-NAME did not affect this enhanced autoregulation in 5-week-old SHR. At perfusion pressures of both 60 and 90 mmHg, 5-week-old SHR showed less coronary NOx- production than age-matched WKY. At 15 weeks, SHR showed a higher blood pressure than WKY. The coronary autoregulation in SHR remained higher than that in WKY, but was below that in 5-week-old SHR. NOx- production in 15-week-old SHR recovered to the level of age-matched WKY. These results indicate that NOx- production induced by mechanical stimulation was markedly reduced in 5-week-old SHR at the prehypertensive stage, which may have enhanced coronary autoregulation. An impaired nitric oxide production may precede the onset of hypertension in SHR. (Hypertens Res 2001; 24: 395-401)
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  • Hitoshi KAWABATA, Teruhiko RYOMOTO, Kinji ISHIKAWA
    2001 Volume 24 Issue 4 Pages 403-409
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    Although angiotensin converting enzyme (ACE) inhibitor and/or angiotensin II type 1 (AT1) receptor antagonist can protect the myocardium against ischemia-reperfusion injury, the mechanisms of the effect have not yet been characterized at the cellular level. We here examined the effect of the combination of an ACE inhibitor, temocaprilat, an AT1 receptor antagonist, CV-11974 and/or a nitric oxide synthase inhibitor, L-NAME, on the myocardial metabolism and contraction during ischemia and reperfusion by using phosphorus 31-nuclear magnetic resonance (31P-NMR) in Langendorff rabbit hearts. After normothermic 20 min global ischemia, postischemic reperfusion of 30 min was carried out. Twenty-one hearts were divided into three experimental groups consisting of 7 hearts each: a Tem+CV group perfused with a combination of temocaprilat and CV-11974; a Tem+CV+L-NAME group perfused with a combination of temocaprilat and CV-11974 plus L-NAME, and a control group. During ischemia, both the Tem+CV group and Tem+CV+L-NAME group showed a significant inhibition of the decrease in adenosine triphosphate (ATP) compared with the control group (p<0.01); the increase in ATP was 50±3%, 42±4%, and 19±4% in the Tem+CV group, Tem+CV+L-NAME group, and control group, respectively. Both experimental groups also showed a significant inhibition of the increase in left ventricular end-diastolic pressure (LVEDP) compared with the control group (p<0.01). After postischemic reperfusion, the Tem+CV group and Tem+CV+L-NAME group again showed a significant improvement of ATP as compared with the control group (p<0.01); the increase in ATP was 73±3%, 64±3%, and 47±4% in the Tem+CV group, Tem+CV+L-NAME group, and control group, respectively, and a significant decrease of LVEDP as compared with the control group (p<0.01). There were no differences in ATP, or LVEDP during ischemia and reperfusion between the Tem+CV group and Tem+CV+L-NAME group. In conclusion, the combination of temocaprilat and CV-11974 showed significant potential for improving myocardial energy metabolism and relaxation during both myocardial ischemia and reperfusion. This beneficial effect was not dependent on NO synthase. (Hypertens Res 2001; 24: 403-409)
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  • Takahito TOMIDA, Yasushi NUMAGUCHI, Hideo MATSUI, Yukio TOKI, Takayuki ...
    2001 Volume 24 Issue 4 Pages 411-419
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    The aim of this study was to evaluate the possible role of prostacyclin (PGI2) in the onset and development of hypertension and chronic renal failure in 5/6-nephrectomized rats (5/6 NX). We measured the systolic blood pressure, 24-h urinary excretion levels of 6-keto-PGF, which was a stable metabolite of PGI2, and levels of PGI2 synthase (PCS) mRNA in the kidneys. Immunostaining for PCS in the kidneys was also evaluated. Systolic blood pressure was higher in 5/6 NX than in sham-operated rats. The 24-h urinary excretion levels of 6-keto-PGF in 5/6 NX at 1 week postsurgery were lower than in sham-operated rats. In renal morphology, tubulointerstitial injury was observed at 2 weeks postsurgery, and glomerulosclerosis at 4 weeks. Levels of PCS mRNA in 5/6 NX decreased significantly at 1 and 2 weeks postsurgery compared with those in sham-operated rats, but at 8 weeks these levels showed a tendency to increase. Immunostaining for PCS was positive in a subset of the cortical thick ascending limb of Henle’s loop cells, including macula densa in both groups. Moreover, in 5/6 NX at 8 weeks postsurgery, mesangial cells also stained positive for PCS. In conclusion, our findings suggest that PCS might play an important role in mitigating glomerular hemodynamic changes associated with reduction of renal mass. (Hypertens Res 2001; 24: 411-419)
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  • Akira NISHIYAMA, Yoshihide FUJISAWA, Toshiki FUKUI, Matlubur RAHMAN, N ...
    2001 Volume 24 Issue 4 Pages 421-427
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    The present study was designed to evaluate the contribution of nitric oxide (NO) to regional hemodynamics during the early phase of angiotensin II (Ang II)-induced hypertension. The responses of regional blood flow to chronic NO synthase inhibition with NG-nitro-L-arginine methyl ester (L-NAME) were assessed using radioactive microspheres in conscious Ang II-infused hypertensive rats. Ang II-infused rats (270 ng/kg/min, subcutaneously for 12 days: n=11) showed higher mean arterial pressure (MAP: 153±4 mmHg) and total peripheral resistance (TPR: 1.61±0.06 mmHg/min/ml), and lower cardiac output (CO: 102±3 ml/min) than vehicle-infused normotensive rats (115±2 mmHg, 0.96±0.05 mmHg/min/ml and 130±7 ml/min, n=11, respectively). The blood flow rates in the brain, spleen, large intestine and skin were significantly reduced in Ang II-infused rats compared with vehicle-infused rats, while those in the lung, heart, liver, kidney, adrenal gland, small intestine, and skeletal muscle were similar. Treating Ang II-infused rats with L-NAME (75 mg/l in drinking water for 10 days, n=11) resulted in higher MAP (166±6 mmHg) and TPR (1.89±0.18 mmHg/min/ml) and lower CO (87±7 ml/min) than untreated Ang II-infused rats. L-NAME-treated Ang II-infused rats showed widespread increases in regional vascular resistance and reduced blood flow rates in the kidney (3.81±0.27 ml/min/g) and skeletal muscle (0.20±0.03 ml/min/g) compared with untreated Ang II-infused rats (6.88±0.27 and 0.33±0.04 ml/min/g, respectively). However, there were no significant differences in the flow rates of other organs investigated between these animals. An NO donor, (±)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (FK409: 30 μg/kg/min, i.v.), significantly decreased MAP (110±6 mmHg) and TPR (1.23±0.18 mmHg/min/ml) without significant changes in CO (89±9 ml/min) in L-NAME-treated Ang II-infused rats. Furthermore, FK409 partially reversed blood flow rates in the kidney (4.72±0.40 ml/min/g) and skeletal muscle (0.25±0.02 ml/min/g) in these animals. These results suggest that NO counteracts, at least in part, the vasoconstrictor effects of elevated Ang II levels in renal and skeletal muscle vascular beds, and is an important modulator in the regulation of blood flow to these organs during the development of Ang II-induced hypertension. (Hypertens Res 2001; 24: 421-427)
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  • Wang YUE, Shoji KIMURA, Yoshihide FUJISAWA, Runxia TIAN, Fanzhu LI, Ma ...
    2001 Volume 24 Issue 4 Pages 429-436
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    The aim of the present study was to determine the effects of benidipine on renal function and whether benidipine may dilate the efferent arteriole as well as the afferent arteriole of the canine kidney. The effects of benidipine on the renal segmental vascular resistance were estimated using Gomez’s formula with some modification. The renal hemodynamic action of benidipine was also compared with that of amlodipine. Intrarenal arterial injection of benidipine at a dose of 3 μg/kg resulted in a significant increase in renal blood flow (RBF), urine flow and urinary excretion of sodium, but not in glomerular filtration rate (GFR). Amlodipine at a dose of 300 μg/kg also increased RBF, urine flow and urinary excretion of sodium to a significant degree equivalent to that by benidipine. However, in contrast to benidipine, amlodipine significantly increased GFR. After the administration of benidipine, autoregulation of RBF and GFR was relatively maintained and the renal perfusion pressure (RPP)-RBF relation shifted upward; that is, RBFs at 75 and 50 mmHg were maintained at a higher level than those of the control. In contrast to benidipine, amlodipine diminished the autoregulation of RBF and GFR. RBFs at 75 and 50 mmHg were not different from those of the control. The afferent and efferent arteriolar resistance (Ra and Re) were calculated based on the RPP-RBF and RPP-GFR relations. Benidipine reduced both Ra and Re, but amlodipine selectively reduced Ra. Benidipine increased RBF but not GFR via the dilation of both afferent and efferent arterioles. Thus, benidipine has unique renal hemodynamic actions which differ from those by most calcium antagonists. (Hypertens Res 2001; 24: 429-436)
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  • Shinji TERAMOTO, Takeo ISHII, Takeshi MATSUSE
    2001 Volume 24 Issue 4 Pages 437-443
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    Factors influencing adeno-associated virus (AAV)-mediated gene transfer to endothelial cells are not fully determined. We tested the variables pertinent to the efficiency of AAV-mediated gene transfer to human vascular endothelial cells (HUVEC) including: (i) kinetics of transduction efficiency of LacZ gene to HUVEC, (ii) the concentration and volume of vector-containing medium, (iii) the period of incubation time of AAV vectors with HUVEC, (iv) the target cell density/proliferation, (v) the duration of transgene expression. There is a dose-response relationship between moi of vectors and transduction efficiency in HUVEC. The higher moi of AAV vectors achieved more than 80% of transduction efficiency in cultured HUVEC. AAV vectors showed incubation time dependent increase in transduction efficiency of LacZ gene to the HUVEC up to 24 h of vector exposure. The foreign gene of AAV vectors preferably transduces the lower density of cells being proliferated. These results indicate that AAV-vector is efficient for gene transfer to HUVEC, and higher moi of vectors or a longer period exposure of vectors to proliferating HUVEC can facilitate efficient transduction of foreign gene into human vascular endothelial cells in vitro. (Hypertens Res 2001; 24: 437-443)
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Case Report
  • Naruya TOMITA, Atsushi MORIGUCHI, Keita YAMASAKI, Yoshiaki TANIYAMA, N ...
    2001 Volume 24 Issue 4 Pages 445-450
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    Von Hippel-Lindau (VHL) disease is an inherited neoplastic disease characterized by a predisposition to develop retinal angiomas, central nervous system hemangioblastomas, renal cell carcinomas, pancreatic cysts and pheochromocytomas. Recently, we encountered three members of the same family who each had both VHL disease and pheochromocytoma. As in all three patients we suspected pheochromocytoma, the diagnosis of VHL disease should be considered. The possible presence of VHL disease was initially investigated in all three patients based on the presence of pheochromocytoma. A mutational analysis of the VHL gene revealed the presence of a missense mutation, consisting of a G to A transversion, at nucleotide 713 in all three patients. This germline point mutation in the VHL gene is often detected in type 2 VHL disease with pheochromocytoma. Genetic analysis seems to be useful for early detection of VHL disease, even when the formal criteria for diagnosis of this disease are lacking. (Hypertens Res 2001; 24: 445-450)
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The Third China and Japan Joint Hypertension Symposium (continued)
Clinical studies
  • Yukio YAMORI, Longjian LIU, Katsumi IKEDA, Ayako MIURA, Shunsaku MIZUS ...
    2001 Volume 24 Issue 4 Pages 453-457
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    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)
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  • Zengwu WANG, Luqin CAO, Yangfeng WU, for the Collaborative Group of C ...
    2001 Volume 24 Issue 4 Pages 459-462
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    It is known that the knowledge, attitude and behavior (KAB) of physicians with respect to hypertension directly affect the prevention of hypertension and associated cardiovascular diseases. To investigate the differences in KAB among cardiologists, neurologists and other physicans, 1,722 potential participants were selected by stratified random sampling. Among these, 1,609 participants took part in the present survey, and 948 of this group were eligible for the present analysis. The data were collected using a self-administrated questionnaire. Results showed that, with respect to knowledge and attitude regarding hypertension, 15.3% of cardiologists, 15.2% of neurologists and 7.2% of other internals selected the correct answers to all questions (p<0.05). The criteria of hypertension were not correctly understood by about two-thirds of physicians, including both cardiologists and neurologists. With regard to behavior, 16.5% of cardiologists, 17.9% of neurologists and 9.6% of other internals selected the correct answers to all questions (p<0.05). A majority of physicians considered that routine blood pressure measurements were not necessary in cases uncomplicated by cardiovascular disease and other disease, such as nephrotic disease, or diabetes mellitus. One-half to two-thirds of physicians did not believe that life style modifications reduce blood pressure. For each question, cardiologists showed the highest, and other internals the lowest, percentage of correct responses to all items in the questionnaire. These findings indicate that cardiovascular health education must be strengthened for all physicians, and not only for specialists. (Hypertens Res 2001;24: 459-462)
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  • Tomohiro KATSUYA, Yoshio IWASHIMA, Ken SUGIMOTO, Motoharu MOTONE, Taka ...
    2001 Volume 24 Issue 4 Pages 463-467
    Published: 2001
    Released: March 29, 2002
    JOURNALS FREE ACCESS
    Many genes and environmental factors are involved in the pathogenesis of hypertension, but the exact cause of essential hypertension has not yet been clarified. Gene polymorphism of the renin-angiotensin system (RAS) is one of the candidates. In the current study, we examined whether there was a correlation between the gene polymorphisms in RAS and either the choice of antihypertensive drugs or their efficacy. Subjects with essential hypertension (n=299) were recruited from among the outpatients of Osaka University Hospital and provided their informed consent for genetic analysis. Physicians freely chose the antihypertensive drugs and adjusted its dose until the patient’s blood pressure was well controlled. The efficacy of each antihypertensive drug was estimated using the following formula: ΔBP=BP 1 (before treatment) - BP 2 (after treatment)/BP 1×100(%). Gene variants in RAS were determined using PCR or PCR-RFLP (restriction fragment of polymorphism). The gene polymorphism of RAS were not associated with ΔSBP or ΔDBP. However, the mean ΔSBP in subjects with a deletion homozygote of the angiotensin converting enzyme gene (ACE/DD) was significantly lower (p<0.05) than that in patients with an insertion/allele of the ACE gene. The gene polymorphisms of RAS did not significantly affect the choice of antihypertensive drugs. Even though gene polymorphism in the renin angiotensin system was not a major factor in the anti-hypertensive therapy, the determination of genotype might be of help in the management of essential hypertension. (Hypertens Res 2001; 24: 463-467)
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