Hypertension Research
Online ISSN : 1348-4214
Print ISSN : 0916-9636
ISSN-L : 0916-9636
Volume 27 , Issue 7
July
Showing 1-11 articles out of 11 articles from the selected issue
Original Articles
Clinical studies
  • Yoshiki YUI, Tetsuya SUMIYOSHI, Kazuhisa KODAMA, Atsushi HIRAYAMA, Hir ...
    2004 Volume 27 Issue 7 Pages 449-456
    Published: 2004
    Released: August 07, 2004
    JOURNALS FREE ACCESS
    We stratified findings from the Japan Multicenter Investigation for Cardiovascular Diseases-B according to whether or not the patients had diabetes and compared the incidence of cardiac events occurring over a 3-year period between treatment with nifedipine retard and angiotensin converting enzyme (ACE) inhibitor. The primary endpoint was the overall incidence of cardiac events (cardiac death or sudden death, myocardial infarction, hospitalization for angina pectoris or heart failure, serious arrhythmia, and coronary interventions), and the secondary endpoints were a composite of other events (cerebrovascular accidents, worsening of renal dysfunction, non-cardiovascular events, and total mortality). The results showed no significant difference in the incidence of the primary endpoint between the nifedipine group (n =199) and the ACE inhibitor group (n =173) in diabetic patients: 15.08% vs. 15.03%, relative risk 1.06, p =0.838. Also in nondiabetic patients, no significant difference was observed between the former (n =629) and the latter (n =649): 13.67% vs. 12.33%, relative risk 1.04, p =0.792. Similar results were obtained for the incidence of the secondary endpoints: in diabetic patients, 5.03% vs. 5.20%, relative risk 0.89, p =0.799; in nondiabetic patients, 2.70% vs. 2.47%, relative risk 1.07, p =0.842. Achieved blood pressure levels were 138/76 and 136/77 mmHg in the nifedipine group and 140/78 and 138/79 mmHg in the ACE inhibitor group in diabetic and nondiabetic patients, respectively. This study showed that nifedipine retard was as effective as ACE inhibitors in reducing the incidence of cardiac events in extremely high-risk hypertensive patients with complications of diabetes and coronary artery disease. (Hypertens Res 2004; 27: 449-456)
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  • Giuseppe DEROSA, Pietro D RAGONESI, Amedeo MUGELLINI, Leonardina CICCA ...
    2004 Volume 27 Issue 7 Pages 457-464
    Published: 2004
    Released: August 07, 2004
    JOURNALS FREE ACCESS
    We evaluated the antihypertensive activity, glucose homeostasis and plasma lipid profile in patients with mild hypertension and type 2 diabetes mellitus treated by diet and exercise, and not in receipt of oral hyperglycemics, following 12-month treatment with either telmisartan or eprosartan. In this double-blind, placebo-controlled trial, 119 patients with mild essential hypertension (diastolic blood pressure [DBP] 91-104 mmHg) and type 2 diabetes were divided into three groups and randomized to receive once-daily telmisartan 40 mg, eprosartan 600 mg, or placebo for 12 months. At enrollment, patients were advised on diet (1,400-1,600 kcal/day) and exercise (physical aerobics on a bicycle for at least 30 min on 4 days each week). Compared with baseline, a significant reduction (p <0.01) in seated trough systolic blood pressure (SBP) was detected after 12-month treatment with either telmisartan or eprosartan. Seated trough DBP was also reduced by telmisartan (p <0.01) and eprosartan (p <0.05); the antihypertensive effect of telmisartan was significantly superior (p <0.05). No change in body mass index or glucose metabolism was observed with either active treatment, or with placebo. Telmisartan, but not eprosartan, significantly improved plasma total cholesterol (p <0.01), low-density lipoprotein cholesterol (p <0.01) and triglycerides (p <0.05) compared with eprosartan. In conclusion, 12-month telmisartan treatment produced a significantly greater reduction in DBP than eprosartan and significantly improved plasma lipids. The improvement could be due to varying pharmacokinetic/pharmacodynamic properties of telmisartan compared with eprosartan, even if it is not clear about the relationship between angiotensin-II receptor blockade and 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibition. (Hypertens Res 2004; 27: 457-464)
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  • Hirofumi TOMIYAMA, Tomio ARAI, Yutaka KOJI, Minoru YAMBE, Kohki MOTOBE ...
    2004 Volume 27 Issue 7 Pages 465-470
    Published: 2004
    Released: August 07, 2004
    JOURNALS FREE ACCESS
    Although blood pressure and age are major determinants of arterial stiffness, it is still unclear whether age-related changes in arterial stiffness are similar among subjects with different degrees of severity of hypertension. The present study examined the association between age and pulse wave velocity in subjects with different degrees of hypertension stratified according to the JNC-7 classification (Normal, Prehypertensive, and Stage I or II Hypertensive subjects). A number of 5,312 subjects (age range, 30-79 years) with no atherosclerotic risk factors other than high blood pressure were selected from two cohorts who regularly underwent annual health checkups, including the measurement of brachial-ankle pulse wave velocity (baPWV). baPWV was increased according to the severity of hypertension in all age groups. The association between age and baPWV formed a quadratic curve in each stage in both genders. The steepness of the slope of the quadratic curve increased according to the severity of hypertension. In each stage of hypertension, age and the baPWV were divided into tertiles. After adjustment for systolic and diastolic blood pressure, the odds ratio of having an increased baPWV in the 3rd age tertile (the highest-age group) was found to increase according to the severity of hypertension. In conclusion, the age-related increase of baPWV was shown to be augmented in phases according to the severity of hypertension, and this augmentation occurred even between the Normal and Prehypertensive stages. These results support the JNC-7 recommendations for a strict control of blood pressure even in the elderly. (Hypertens Res 2004; 27: 465-470)
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  • Katsuhiko KOHARA, Yasuharu TABARA, Rieko TACHIBANA, Jun NAKURA, Tetsur ...
    2004 Volume 27 Issue 7 Pages 471-477
    Published: 2004
    Released: August 07, 2004
    JOURNALS FREE ACCESS
    Microalbuminuria is an early marker of renal damage and has been shown to predict future cardiovascular mortality and morbidity in patients with diabetes or hypertension, as well as in subjects in the general population. In this study, we investigated the hypothesis that the presence of microalbuminuria reflects the advancement of arterial stiffness by using a study group of 136 community residents who had no cardiovascular diseases except for hypertension and who were not taking any medications. Urinary albumin concentration was determined by the standard method and corrected by creatinine. Microalbuminuria was defined as a urinary albumin/creatinine ratio of 2.0-30.0 mg/mmol creatinine. Arterial stiffness was evaluated by pulse wave velocity (PWV) determined at three points: from the heart to the carotid artery, to the brachial artery, and to the ankle. Carotid arterial pressure was determined using a tonometric sensor. Carotid ultrasonography was performed to measure carotid intima-media thickness (IMT) and carotid arterial internal dimension. Subjects with microalbuminuria had higher blood pressure and wider pulse pressure not only in the brachial artery but also in the carotid artery. Microalbuminuria was associated with significantly higher PWV compared with that of normoalbuminuric subjects at all sites studied (mean PWV: 821.2±137.4 cm/s vs. 933.8±137.5 cm/s, p <0.0001). Stepwise regression analysis revealed that the presence of mircroalbuminuria (p =0.047) was a significant independent predictor of PWV in addition to age, sex, and systolic blood pressure. These findings suggest that microalbuminuria is associated with advanced atherosclerosis in the general population. Underlying arterial stiffness may explain the high cardiovascular mortality in subjects with microalbuminuria. Hypertension may be the mechanism linking microalbuminuria and arterial stiffness in the general population. (Hypertens Res 2004; 27: 471-477)
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  • Takeshi TANIGAWA, Naoko TACHIBANA, Kazumasa YAMAGISHI, Isao MURAKI, Mi ...
    2004 Volume 27 Issue 7 Pages 479-484
    Published: 2004
    Released: August 07, 2004
    JOURNALS FREE ACCESS
    To examine the relationship between sleep-disordered breathing (SDB) and blood pressure levels among Japanese men, we conducted a population-based cross-sectional study of 1,424 men aged 40-69 years in rural and urban communities. The 3% oxygen desaturation index (ODI) was selected as the indicator of SDB, representing the number of desaturation events per hour of recording time in which blood oxygen fell by ≥3% according to overnight pulse oximetry. To estimate the associations of 3% ODI levels with blood pressure levels and hypertension, multiple linear regression and logistic regression analyses were performed. The 3% ODI level was positively associated with systolic and diastolic blood pressure levels (SBP/DBP); a 5 event per hour increment of the 3% ODI level was associated with 0.8 mmHg (95% confidence interval [CI], 0.0-1.6) greater SBP and 0.7 mmHg (95% CI, 0.3-1.1) greater DBP after adjustment for age, body mass index, ethanol intake, smoking category and community. The multivariate odds ratio of hypertension for the low vs. high category of 3% ODI level was 1.63 (95% CI, 1.1-2.5). These associations were more evident among overweight than non-overweight individuals. The significant association of nocturnal oxygen desaturation with high blood pressure levels suggests that SDB plays a role in the development of hypertension among Japanese men. (Hypertens Res 2004; 27: 479-484)
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Experimental studies
  • Masaichi-Chang-il LEE, Hirofumi SHOJI, Hiroyuki MIYAZAKI, Fumihiko YOS ...
    2004 Volume 27 Issue 7 Pages 485-492
    Published: 2004
    Released: August 07, 2004
    JOURNALS FREE ACCESS
    This study examined the blood brain barrier (BBB)-permeable nitroxyl compound, 3-methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl (MC-PROXYL), as a spin probe for the assessment of oxidative stress in the brain by electron spin resonance (ESR) imaging and in vivo L-band ESR. Preliminary comparisons were made by ESR imaging of MC-PROXYL in the isolated brains of normal Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke prone SHR (SHRSP). The decay of the ESR images of MC-PROXYL in the isolated brains was faster in SHR than in normal WKY, but was only moderate in SHRSP. In addition, the decay rate of MC-PROXYL in the heads of live rats, as measured noninvasively by L-band ESR, was faster in SHR than in WKY, and was slower in SHR than in SHRSP. Taken together, our data suggest that the oxidative stress of SHR is not as high as that in high oxidative stress animal models such as SHRSP. This is the first study to present reconstructed 3D images of the distribution of MC-PROXYL in the isolated SHR brain. The ESR technique employed herein appears to be a powerful tool for evaluating oxidative stress and for detecting the region of oxidative stress in the brain of SHR. (Hypertens Res 2004; 27: 485-492)
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  • Li YAO, Hiroyuki KOBORI, Matlubur RAHMAN, Dale M SETH, Takatomi SHOKOJ ...
    2004 Volume 27 Issue 7 Pages 493-500
    Published: 2004
    Released: August 07, 2004
    JOURNALS FREE ACCESS
    Recent studies have indicated that both endothelin (ET) and angiotensin (Ang) II stimulate oxidative stress, which contributes to the development of hypertension. Here, we examined the effects of Ang II type 1 (AT1) receptor blockade on reactive oxygen species (ROS) formation in ET-dependent hypertension. Chronic ET-1 infusion (2.5 pmol/kg/min, i.v., n =7) into rats for 14 days increased systolic blood pressure from 113±1 to 141±2 mmHg. ET-1-infused rats showed greater plasma renin activity (8.1±0.8 Ang I/ml/h), and greater Ang I (122±28 fmol/ml) and Ang II levels (94±13 fmol/ml) than vehicle (0.9% NaCl)-infused rats (3.1±0.6 Ang I/ml/h, 45±8 and 47±7 fmol/ml, respectively, n =6). Angiotensin converting enzyme and AT1 receptor expression in aortic tissues were similar between the vehicle- and ET-1-infused rats. Vascular superoxide anion (O2-) production and plasma thiobarbituric acid-reactive substance (TBARS) levels were greater in ET-1-infused rats (27±1 counts per minutes [CPM]/mg dry tissue weight and 8.9±0.8μmol/l, respectively) than vehicle-infused rats (16±1 CPM/mg and 5.1±0.1μmol/l, respectively). The ET-1-induced hypertension was prevented by simultaneous treatment with a new AT1 receptor antagonist, olmesartan (0.01% in chow, 117±5 mmHg, n =7), or hydralazine (15 mg/kg/day in drinking water, 118±4 mmHg, n =6). Olmesartan prevented ET-1-induced increases in vascular O2- production (15±1 CPM/mg) and plasma TBARS (5.0±0.1μmol/l). Vascular O2- production and plasma TBARS were also decreased by hydralazine (21±1 CPM/mg and 7.0±0.3μmol/l, respectively), but these levels were significantly higher than in vehicle-infused rats. These data suggest that ET-dependent hypertension is associated with augmentation of Ang II levels and ROS formation. The combined effects of the elevations in circulating ET-1 and Ang II, as well as the associated ROS production, may contribute to the development of hypertension induced by chronic ET-1 infusion. (Hypertens Res 2004; 27: 493-500)
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  • Koichi HASEGAWA, Hideaki YOSHIDA, Nobuyuki URA, Hideyuki MURAKAMI, Mak ...
    2004 Volume 27 Issue 7 Pages 501-508
    Published: 2004
    Released: August 07, 2004
    JOURNALS FREE ACCESS
    Insulin resistance and impairment of the renal depressor system have been thought to be involved in the development of essential hypertension. However, the relationship between insulin resistance and this system is still unclear. To clarify this relationship, we investigated the role of the renal depressor system in a rat model of insulin-resistant hypertension. Sprague-Dawley rats were fed a standard diet (control) or a fructose-rich diet (FFR), and their blood pressures were measured every week. Urinary dopamine (uDA), urinary kallikrein (uKAL) activity and urinary nitric oxide (uNOx) levels were also measured each week, and the renal mRNA expression levels of endothelial nitric oxide synthase (eNOS), aromatic-L-amino-acid decarboxylase (AADC), and kallikrein (KAL) activity were compared at the end of the study. The blood pressure of FFR was elevated significantly from 2 weeks after the start of fructose loading. The uDA level was lower in FFR than in control rats throughout the study period (p <0.01), and the expression level of AADC mRNA was enhanced in FFR (p <0.05). There was a tendency of negative correlation between uDA level and systolic blood pressure (SBP) (r =-0.49, p =0.056). uNOx level was lower in FFR throughout the study period (p <0.05), and the eNOS mRNA expression level in the kidney was lower in FFR than in control rats (p <0.05). There was a negative correlation between uNOx level and SBP (r =-0.68, p <0.01). On the other hand, there was no significant difference in the kallikrein-kinin system between FFR and control rats. In conclusion, impairment in functions of the renal dopamine and NO systems occur in FFR, and this impairment may be caused by insulin resistance and may contribute to the development of hypertension. (Hypertens Res 2004; 27: 501-508)
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  • Masayuki KANAZAWA, Masahiro KOHZUKI, Hajime KUROSAWA, Naoyoshi MINAMI, ...
    2004 Volume 27 Issue 7 Pages 509-515
    Published: 2004
    Released: August 07, 2004
    JOURNALS FREE ACCESS
    To assess the renal benefits of combined angiotensin-converting enzyme inhibition and α1-adrenergic antagonism, we studied the antihypertensive and renoprotective effects of temocapril (TMP) alone and in combination with doxazosin (DOX) in spontaneously hypertensive rats (SHR)/Izumo rats with renal ablation. Five-Sixths-nephrectomized rats were assigned to receive TMP (10 mg/kg/day) (TMP group), TMP plus DOX (2 mg/kg/day) (TMP+DOX group), or vehicle (control group) orally for 12 weeks. Both systolic blood pressure (SBP) and urinary excretion of albumin (UalbV) in the control group progressively increased during the experimental period and were significantly higher than in sham-operated rats. Treatment with either TMP or TMP plus DOX had similar antihypertensive effects in this rat model. Twelve weeks after initiation of treatment, the SBP values in the control, TMP, and TMP+DOX groups were 265±8, 157±4, and 163±3 mmHg, respectively, in comparison with 233±4 mmHg in sham-operated rats (p <0.0001 control vs. sham, p <0.001 TMP vs. control, p <0.001 TMP+DOX vs. control). UalbV, serum creatinine (Scr), blood urea nitrogen (BUN), and heart weight/body weight (HW/BW) ratio were significantly lower in the TMP and TMP+DOX groups than in the control group (UalbV: p <0.05; Scr: p <0.01; [BUN, HW/BW ratio]: p <0.0001; and [UalbV, Scr, BUN, HW/BW ratio]: p <0.0001 vs. control, respectively). The index of glomerular sclerosis (IGS) and relative interstitial volume (RIV) were significantly lower in the TMP+DOX group than in the control group (IGS: p <0.05; RIV: p <0.01). Especially, UalbV, IGS, and RIV were significantly better in the TMP+DOX group than in the TMP group ([IGS, RIV]: p <0.05; UalbV: p <0.01). These results suggest that simultaneous administration of TMP and DOX provides greater renoprotective effects than administration of TMP alone. (Hypertens Res 2004; 27: 509-515)
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  • Shinji TAKAI, Denan JIN, Masato SAKAGUCHI, Michiko MURAMATSU, Kenji IS ...
    2004 Volume 27 Issue 7 Pages 517-522
    Published: 2004
    Released: August 07, 2004
    JOURNALS FREE ACCESS
    Angiotensin II receptor blockers could prevent the development of atherosclerosis beyond reducing blood pressure in monkeys fed a high-cholesterol diet. However, it has been unclear whether hypotensive effects improve atherosclerosis in primates. We investigated whether antihypertensive agents, an angiotensin II receptor antagonist, candesartan, and a calcium channel blocker, amlodipine, prevent areas of atherosclerotic lesions in the aorta of monkeys fed a high-cholesterol diet. Seventeen male monkeys fed a high-cholesterol diet for 6 months were grouped as follows: a high-cholesterol diet group (n =5), a candesartan-treated group (1 mg/kg per day, n =6) and an amlodipine-treated group (5 mg/kg per day, n =6). Candesartan and amlodipine showed a similar hypotensive effect by decreasing the systolic blood pressure approximately 20 mmHg, while these agents did not affect serum cholesterol levels. The ratio of atherosclerotic area to total area in thoracic aorta was significantly decreased by treatment with candesartan, but the ratio tended to be decreased by treatment with amlodipine. Although the angiotensin-converting enzyme activity in plasma was not changed by treatment with candesartan or amlodipine, the angiotensin-converting enzyme activity in the thoracic aorta was obviously reduced by treatment with candesartan, but not with amlodipine. Therefore, a blockade of angiotensin II action rather than a hypotensive effect may play an important role in preventing the development of atherosclerosis in primates. (Hypertens Res 2004; 27: 517-522)
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Case Report
  • Tetsuro YOSHIDA, Noriyuki IKEHARA, Hiromichi MIYABE, Seiichiro SAKATA, ...
    2004 Volume 27 Issue 7 Pages 523-526
    Published: 2004
    Released: August 07, 2004
    JOURNALS FREE ACCESS
    We experienced two cases of renal infarction with atrial fibrillation who presented with acute abdominal pain. On initial urinalysis, both patients showed no hematuria, but the plasma lactate dehydrogenase level was markedly elevated with little or no rise in plasma transaminases. Their diagnosis was confirmed by contrast-enhanced CT of the abdomen on the second and third days of the crisis. We immediately initiated anticoagulant therapy, resulting in successful prevention of new embolism. Contrast-enhanced CT should be considered if abdominal symptoms develop in patients with atrial fibrillation. Renal infarction could be diagnosed in the early course, even in cases with incomplete occlusion of the renal arteries and normal renal function. (Hypertens Res 2004; 27: 523-526)
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