Hypertension Research
Online ISSN : 1348-4214
Print ISSN : 0916-9636
ISSN-L : 0916-9636
26 巻 , 5 号
May
選択された号の論文の12件中1~12を表示しています
Reviews
  • Trefor MORGAN
    原稿種別: Review
    2003 年 26 巻 5 号 p. 349-354
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    Angiotensin II and sodium balance affect the status of each other and both—either separately or together—can lead to an increase in blood pressure. They also can cause vascular and cardiac damage due to direct effects and effects mediated by the blood pressure increase. This paper reviews the important interactions among these three variables. Acute blood pressure elevation during sleeping but not during waking hours causes cardiac hypertrophy in rats. Similarly, lowering of blood pressure with an angiotensin converting enzyme (ACE) inhibitor during sleep but not when awake causes regression of cardiac hypertrophy in rats with 2 kidney (K)-1 clip (C) Goldblatt hypertension. If angiotensin is given to rats on a low (0.4%) NaCl diet, blood pressure rises but there is less cardiac hypertrophy. Cardiac hypertrophy is greatest after angiotensin administration in rats on a high (4%) NaCl diet. In both the 2K-1C and 1K-1C Goldblatt models, a high salt intake reduces the blood pressure lowering effect of captopril and losartan and prevents regression of cardiac hypertrophy. Combined administration of an ACE inhibitor and an angiotensin type 1 (AT1) receptor blocker to rats on a low (0.2%) NaCl diet produces a syndrome that leads to death with cardiac involution. All features of the syndrome are reversed or prevented by 4% NaCl intake. It is hypothesised that the interaction between angiotensin II and sodium intake can be explained by differences in the way protons produced by contracting cells are neutralized. The sodium hydrogen exchanger and the sodium 2 bicarbonate cotransporter are stimulated by the AT1 and angiotensin type 2 (AT2) receptor, respectively. If the ratio of receptors is altered in favour of the AT2 receptor, then less cardiac hypertrophy will result from the same workload. Review of the clinical literature reveals that many of these results in rats have correlations in clinical medicine. Thus high night time blood pressure is associated with a greater morbidity and high salt intake causes cardiac hypertrophy and vascular stiffness independent of blood pressure levels. When deciding on treatment in human hypertension these results have important clinical implications. (Hypertens Res 2003; 26: 349-354)
  • Kazuomi KARIO, S. McEWEN Bruce, G. PICKERING Thomas
    原稿種別: Review
    2003 年 26 巻 5 号 p. 355-367
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    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)
Original Articles
Clinical studies
  • Hiroyuki SUMINO, Shuichi ICHIKAWA, Hisao KUMAKURA, Yoshiaki TAKAYAMA, ...
    原稿種別: Original Article
    専門分野: Clinical studies
    2003 年 26 巻 5 号 p. 369-376
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    No study has demonstrated that hormone replacement therapy (HRT) affects blood pressure (BP) measured by 24-h ambulatory blood pressure monitoring (ABPM) in Japanese postmenopausal women (PMW) with normotension or mild-to-moderate essential hypertension. In the present study, we examined the effects of HRT on office BP and 24-h ambulatory blood pressure (ABP) in Japanese hypertensive or normotensive PMW. Thirty-one hypertensive (HT-HRT group) and 17 normotensive PMW (NT-HRT group) received HRT (0.625 mg of conjugated equine estrogen combined with 2.5 mg of medroxyprogesterone acetate) orally for 12 months, and 30 hypertensive (HT-Control group) and 19 normotensive PMW (NT-Control group) did not receive HRT. In all of the hypertensive PMW, BP was controlled by a variety of antihypertensive drugs before starting HRT. The hypertensive PMW were divided into two groups according to the results of ABP before HRT: nondippers (those without a diurnal change in BP) and dippers (those with a diurnal change in BP). In all patients, office BP measurements and 24-h ABPM were performed before and 12 months after the start of HRT. HRT did not change either the office or the 24-h ambulatory systolic, diastolic, or mean BP in any of the groups. Therefore, HRT did not significantly alter the proportion of nondippers. We conclude that with respect to BP, HRT might not be harmful in hypertensive PMW whose BP has been well-controlled prior to the initiation of HRT, as well as in normotensive PMW. (Hypertens Res 2003; 26: 369-376)
  • Renzhe CUI, Hiroyasu ISO, Kazumasa YAMAGISHI, Takeshi TANIGAWA, Hirono ...
    原稿種別: Original Article
    専門分野: Clinical studies
    2003 年 26 巻 5 号 p. 377-382
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    Low ankle-arm systolic blood pressure index (AAI) correlates with various cardiovascular risk factors and with risk of subsequent coronary heart disease and stroke in Western countries. However, few epidemiological data are available among Japanese, in whom the reported prevalence of peripheral artery disease is low. We examined the relationship between AAI and cardiovascular risk factors among 1, 219 men aged 60 to 79 years in two Japanese communities in 1999 and 2000. The prevalence of AAI<0.90 was 5% in both communities. Hypertension, major ECG abnormality, current smoking, and history of stroke were associated with two- to four-fold higher prevalence of AAI<0.90. One-standard deviation increments of body mass index and high density lipoprotein-cholesterol levels were associated with 60% and 40% lower prevalence of AAI<0.90, respectively. Although the prevalence of low AAI in Japanese elderly men is lower than that reported in the Unites States and European studies, similar correlations of low AAI with cardiovascular risk factors were observed among different ethnic groups. Low AAI is suggested to be a predictor for stroke among Japanese men, which should be confirmed by a prospective study. (Hypertens Res 2003; 26: 377-382)
  • Shinji YAGI, Seiichi GOTO, Taro YAMAMOTO, Susumu KURIHARA, Shigehiro K ...
    原稿種別: Original Article
    専門分野: Clinical studies
    2003 年 26 巻 5 号 p. 383-387
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    To clarify the effect of cilnidipine, a long-acting dihydropyridine Ca-antagonist that blocks both L- and N-type Ca2+-channels, on insulin sensitivity, cilnidipine at 5 to 10 mg/day was administered to ten patients with essential hypertension for 12 weeks. Mean age and body mass index (BMI) were 57.7±5.0 (SEM) years old and 27.1±1.5, respectively. Blood pressure, serum levels of catecholamines, glucose and lipid were determined before and after the treatment. Insulin sensitivity was also measured by a euglycemic hyperinsulinemic clamp method using an artificial pancreas (STG-22; Nikiso, Tokyo, Japan) before and after the treatment. Cilnidipine administration significantly lowered blood pressure from 154/96 to 137/84 mmHg (p <0.05). The glucose infusion rate was significantly increased by 20.8%, from 3.27±0.36 to 3.95±0.55 mg/kg/min (p <0.05). HbA1C and serum lipid levels such as total cholesterol and triglyceride were not altered. In addition, cilnidipine treatment did not significantly increase serum norepinephrine levels (278±25.2 vs. 332±33.6 pg/ml). Our results suggest that cilnidipine improves insulin sensitivity, possibly due to its exerting a vasodilatory action without stimulating sympathetic nervous activity. (Hypertens Res 2003; 26: 383-387)
Experimental studies
  • Koichi YAMAGUCHI, Katsuhiro HIGASHIURA, Nobuyuki URA, Hideyuki MURAKAM ...
    原稿種別: Original Article
    専門分野: Experimental studies
    2003 年 26 巻 5 号 p. 389-396
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    Recent studies have indicated that tumor necrosis factor (TNF)-α plays a significant role in insulin resistance. It has been proposed that selective impairment of insulin signaling in glucose metabolism is related to the development of atherosclerosis, although the mechanisms are not clear. The aim of this study was to elucidate the effect of TNF-α on tissue specificity and selectivity to insulin signaling. L6 myotubes and rat aortic vascular smooth muscle cells (VSMC) were cultured. Cells were stimulated with insulin pretreated with or without TNF-α. The protein extracts were used for electrophoresis and immunoblotting studies to examine phosphorylation of insulin receptor (IR)-β, insulin receptor substrate (IRS)-1 and extracellular signal-regulated kinase (ERK). IR-β phosphorylation was not affected by TNF-α in L6 or in VSMC. TNF-α significantly (p <0.05) inhibited IRS-1 phosphorylation by insulin but had no effect on ERK in L6. TNF-α had no effect on either IRS-1 phosphorylation or ERK in VSMC. Insulin induced ERK phosphorylation in a dose-dependent manner in VSMC. These results suggests that TNF-α plays a significant role in the tissue specificity and signal selectivity of insulin resistance. The pathway related to glucose metabolism is selectively impaired by TNF-α in skeletal muscle, and this impairment may induce compensatory hyperinsulinemia, which in turn would stimulate the pathway related to the cell proliferation in vascular tissues and possibly enhance the progression of atherosclerosis. (Hypertens Res 2003; 26: 389-396)
  • Martina VOKURKOVÁ, Zdena DOBEŠOVÁ, Jaroslav KUNE& ...
    原稿種別: Original Article
    専門分野: Experimental studies
    2003 年 26 巻 5 号 p. 397-404
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    The possible association of salt hypertension and altered lipid metabolism with abnormalities of particular systems transporting sodium and potassium has been studied in erythrocytes of Dahl rats and their F2 hybrids fed a high-salt diet since weaning. Our attention was paid to the Na+-K+ pump, Na+-K+ cotransport and especially to passive membrane permeability for Na+ and Rb+ (Na+ and Rb+ leak), because the Na+ leak was found to be dependent on the genotype, age and salt intake of Dahl rats, whereas the Rb+ leak was suggested to be a potential marker of salt sensitivity in Dahl and Sabra rats. Young male Dahl salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) rats kept on a low-salt (0.3% NaCl) or high-salt diet (8% NaCl) were used for the progenitor study. The subsequent genetic study was based on 135 young male SS/Jr×SR/Jr F2 hybrids fed a high-salt diet since weaning. Ouabain (5 mmol/l) and bumetanide (10μmol/l) were used to distinguish the contribution of the Na+-K+ pump, Na+-K+ cotransport and passive membrane permeability to measured net Na+ fluxes and unidirectional Rb+ (K+) movements. Compared to normotensive SR/Jr animals, salt-loaded SS/Jr rats had higher blood pressure (BP), elevated erythrocyte Na+ content, and increased Na+ and Rb+ leaks together with enhanced Na+ and Rb+ transport mediated by the Na+-K+ pump and Na+-K+ cotransport system. Salt hypertensive Dahl rats were also characterized by elevated plasma levels of total cholesterol and triglycerides, which were positively associated with BP of F2 hybrids (r =0.27 and 0.24, p <0.01). In F2 hybrids, mean arterial pressure correlated significantly with erythrocyte Na+ content (r =0.24, p <0.01) and ouabain-sensitive Na+ extrusion, but not with the passive membrane permeability for Na+ or Rb+ (r =-0.02 and 0.06, not significant). Both of the above-mentioned significant associations could partially be ascribed to the dependence of erythrocyte Na+ content and ouabain-sensitive Na+ extrusion on plasma cholesterol (r =0.18 and 0.21, p <0.05). Our results support the idea that abnormal lipid metabolism and/or altered Na+, K+-ATPase function play an important role in the pathogenesis of salt hypertension in salt-sensitive Dahl rats. (Hypertens Res 2003; 26: 397-404)
  • Ken IMANISHI, Hiroshi NONOGUCHI, Yushi NAKAYAMA, Kenji MACHIDA, Mika I ...
    原稿種別: Original Article
    専門分野: Experimental studies
    2003 年 26 巻 5 号 p. 405-411
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    Angiotensin II plays important roles in renal vasoconstriction, sodium reabsorption in proximal tubules, and cell proliferation. Angiotensin II receptors are present not only in proximal but also in distal tubules. We investigated the effects of dehydration on the mRNA expression of type 1A angiotensin II receptor (AT1A) in proximal and distal nephron segments and on the expression of type 1 angiotensin II receptor (AT1) protein. Competitive polymerase chain reaction was employed to quantitatively examine mRNA expression, and AT1-specific polyclonal antibody was used for Western blot analysis. AT1A mRNA expression was most abundant in glomeruli. Collecting ducts showed higher expressions than did proximal tubules or thick ascending limbs. Dehydration caused an increase of AT1A mRNA expression in glomeruli, proximal straight tubules (PST), and medullary and cortical thick ascending limbs (MAL and CAL, respectively). In contrast, dehydration decreased AT1A mRNA expression in cortical, outer medullary, and inner medullary collecting ducts (CCD, OMCD, and IMCD, respectively). Incubation of isolated glomeruli, PST, and IMCD in hypertonic solution made by NaCl and mannitol in vitro increased AT1A mRNA expression. Incubation of IMCD with AVP (10-7 mol/l) also increased AT1A mRNA expression. AT1 was detected at 45 kDa by Western blotting. Dehydration caused a decrease and increase of AT1 expression in the cortex and the medulla, respectively. In summary, these data showed that the mechanisms of the regulation of AT1A differ between proximal and distal tubules. The finding that AT1 was up-regulated in the medulla during dehydration may suggest that this receptor plays an important role in dehydration in the distal tubules. (Hypertens Res 2003; 26: 405-411)
  • Akihiro TOJO, Maristela Lika ONOZATO, Hidetake KURIHARA, Tatsuo SAKAI, ...
    原稿種別: Original Article
    専門分野: Experimental studies
    2003 年 26 巻 5 号 p. 413-419
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    The kidney plays an important role in protein metabolism. The albumin reabsorption in the proximal tubule is disturbed in the early stage of diabetic nephropathy. We evaluated the effects of angiotensin converting enzyme inhibitor (ACEI) and angiotensin II type 1 receptor blocker (ARB) on albumin reabsorption and expression of megalin, an endocytosis receptor for albumin, in proximal tubules of streptozotocin (STZ)-induced diabetic-rats. Diabetic rats at the second week after STZ injection were treated with quinapril (3mg/kg/day) or candesartan (0.05mg/kg/day) for 2 weeks. The tubular reabsorption of fluorescein isothiocyanate (FITC)-labeled albumin was evaluated by immunogold electron microscopy, and megalin expression was investigated by immunohistochemistry and Western blotting. Reabsorption of FITC-labeled albumin and megalin expression were prominently inhibited in the proximal convoluted tubules of diabetic rats compared to the controls. Both quinapril and candesartan restored albumin reabsorption in the proximal tubule due to normalization of megalin expression. Urinary albumin excretion was significantly reduced by both ACEI and ARB treatment. Angiotensin II infusion decreased megalin expression and albumin reabsorption in the proximal tubule. In conclusion, angiotensin II blockade restored albumin reabsorption via amelioration of megalin expression in the proximal tubules of early stage diabetic rats. (Hypertens Res 2003; 26: 413-419)
  • Yuichi KOIDE, Kouichi TAMURA, Atsushi SUZUKI, Kouichi KITAMURA, Keiko ...
    原稿種別: Original Article
    専門分野: Experimental studies
    2003 年 26 巻 5 号 p. 421-426
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    Several protein kinase C (PKC) isoforms may play important roles in cellular signaling pathways. Recent reports have suggested that PKC plays critical isoform-specific roles in the development of cardiac hypertrophy and heart failure. The purpose of the present study was to examine the expression profiles of PKC isoforms in models of cardiac hypertrophy and heart failure. We examined the cardiac expression of individual PKC isoforms at the cardiac hypertrophy stage and the heart failure stage in Dahl salt-sensitive rats by Western blot analysis. The levels of all PKC isoforms increased at the cardiac hypertrophy stage and the heart failure stage, but the pattern of increase differed among PKC isoforms at the heart failure stage. The expressions of PKCα, β, and δ increased at the cardiac hypertrophy stage and remained elevated at the heart failure stage. On the other hand, the expression of PKCε and atypical PKCs (aPKCs) increased at the cardiac hypertrophy stage, but this increase tended to decline at the congestive heart failure stage. These results suggest that there are two groups of PKC isoforms. Several reports have shown that PKCα, β, and δ are involved in the development of cardiac hypertrophy and heart failure, and that PKCε plays a role in the physiological hypertrophic responses and cardioprotective actions. These facts suggest that all PKC isoforms (PKCα, β, δ, ε, and aPKCs) expressed in the heart may have similar functions at the cardiac hypertrophy stage, but that two groups of PKC isoforms (PKCα, β, δ, and PKCε, aPKCs) have different functions at the congestive heart failure stage. (Hypertens Res 2003; 26: 421-426)
  • Yi ZHANG, G. SCHYVENS Christopher, U.S. McKENZIE Katja, J. MORRIS Bria ...
    原稿種別: Original Article
    専門分野: Experimental studies
    2003 年 26 巻 5 号 p. 427-432
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    Lipopolysaccharide (LPS) was used to stimulate nitric oxide (NO) release and investigate the effect of endogenous NO on adrenocorticotrophic hormone (ACTH)-induced hypertension in rats. After preliminary studies to determine the appropriate dose of LPS, 40 male Sprague-Dawley rats were treated with ACTH (200 μg/kg/day, s.c.) or saline (sham) for 8 days and then given a single dose of LPS (10 mg/kg, i.p.) or saline. ACTH treatment was continued for a further 5 days. Systolic blood pressure (SBP) was measured daily using the tail cuff method. Results were expressed as the mean±SEM. ACTH treatment significantly increased SBP (from 105±3 to 129±4 mmHg; p <0.05), whereas saline had no effect on SBP. The ACTH-induced increase in SBP was reversed by LPS injection (from 125±6 to 102±7 mmHg; p <0.05). SBP was also decreased in sham + LPS-treated rats compared with that of sham + saline-treated rats (p <0.05), but the SBP change in response to LPS was greater in ACTH-treated than in sham-treated rats (-23 vs. -8 mmHg; p <0.05). These data are compatible with the notion that reduced NO availability plays a role in ACTH-induced hypertension. (Hypertens Res 2003; 26: 427-432)
Case Report
  • Toshihiro KITA, Takuroh IMAMURA, Haruhiko DATE, Kazuo KITAMURA, Sayaka ...
    原稿種別: Case Report
    2003 年 26 巻 5 号 p. 433-437
    発行日: 2003年
    公開日: 2003/12/10
    ジャーナル フリー
    We report two cases of pheochromocytoma combined with tetralogy of Fallot who showed different clinical courses. Case 1 was a 45-year-old woman with a history of radical operation for tetralogy of Fallot at 20 years of age. She presented with sudden hypertensive attack, and was diagnosed with pheochromocytoma of the left adrenal gland. She was treated surgically, and her high plasma noradrenaline level normalized. Case 2 was a 41-year-old woman who had been suffering from severe cyanosis due to tetralogy of Fallot throughout her life. A palliative operation had been performed at 7 years of age, but a radical operation had not been performed. She has had resistant hypertension since 38 years of age. She was diagnosed as having pheochromocytoma of the left adrenal gland at 41 years of age, but surgery was not performed. She was pharmacologically treated with doxazosin, followed by bisoprolol. Her symptoms somewhat improved, although she continued to have high plasma levels of noradrenaline and adrenomedullin. The combination of pheochromocytoma with tetralogy of Fallot or cyanotic congenital heart disease is rare; however, pheochromocytoma and congenital heart disease might be related through chronic hypoxia and/or gene abnormalities. The presence of pheochromocytoma worsens the hemodynamic state in patients with congenital heart disease regardless of whether radical surgery for congenital heart disease had been performed. Differential diagnosis of pheochromocytoma could be paramount in congenital heart disease patients who show unexpected or unusual symptoms. (Hypertens Res 2003; 26: 433-437)
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