Several dietary factors have been shown to lower blood pressure in elderly patients in clinical trials, but it is not known how eating habits affect blood pressure control in outpatients treated with antihypertensive drugs. We obtained data on dietary information regarding food groups rich in potassium, magnesium, and calcium by submitting a questionnaire to 190 elderly outpatients. Blood pressure levels and the intensity and cost of antihypertensive treatment were obtained from clinical records. The mean age and blood pressure were 72.3±9.3 years and 138.7±15.2/74.6±8.8mmHg, respectively. Patients were divided into three groups on the basis of the intensity of medication: the LS group (n=52), treated with a low dose of a single drug; the HS group (n=95), treated with a high dose of a single drug; and the M group (n=43), treated with multiple drugs. Average age, body mass index, blood pressure levels, and extent of target organ damage were similar among the three groups. Intake frequency (rarely, once or twice per week, 3 to 6times per week, or every day) of the food groups was compared among the three groups. The LS group ate fruit (p<0.05) and seaweed (p<0.01) with significant frequency compared with the other groups, whereas milk and dairy products were taken with similar frequency by all groups. The monthly cost of antihypertensive medications averaged ¥17, 218±620 in the LS group, ¥17, 746±375 in the HS group, and ¥20, 066±1, 364 in the M group. These data suggest that habitual intake of foods rich in potassium and magnesium are associated with reduced intensity and cost of medication and with preservation of blood pressure control in elderly hypertensive outpatients. (Hypertens Res 2000; 23:195-200)

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Blood pressure has been shown to decrease in response to hospital admission. Several parameters including the decline of sympathetic nervous activity and negative sodium balance have been shown to be involved in this phenomenon. We investigated genetic influence on office BP and BP after hospitalization. One hundred and sixty-three men from the general population, free from antihypertensive medication, were enrolled in the present study. They stayed at the hospital for general medical check-up. BP was measured on the day of admission, and again the following day. Mean systolic blood pressure was significantly decreased after hospitalization from 117.3±9.9mmHg to 115.3±12.8mmHg (p=0.042). Subjects with DD+ID genotype showed a significantly higher systolic blood pressure after hospitalization than that of subjects with genotype II. There were no genotype specific differences in diastolic blood pressure or changes in blood pressure by the administration. In summary, systolic blood pressure after hospitalization was significantly higher in normotensive male subjects who possessed the D allele of ACE I/D polymorphism. (Hypertens Res 2000; 23: 201-205)

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We determined the changes in blood pressure, pulse rate, and heart rate variability during dental surgery in hypertensive patients. The study included 18 essential hypertensives and 18 age and sex matched normotensive controls who underwent tooth extraction at our hospital. Holter electrocardiographic monitoring was used to determine the power spectrum of R-R variability before and during dental surgery. The low frequency (LF: 0.041 to 0.140Hz), high frequency (HF: 0.140 to 0.500Hz), and total spectral powers (TF: 0.000 to 4.000Hz) were calculated, and the ratio of LF to HF and the percentage of HF relative to TF (%HF: HF/TF×100) were used as indexes of sympathetic and parasympathetic activities, respectively. The baseline blood pressure for hypertensive patients (149±4/85±2mmHg) was significantly higher than that for normotensive patients (119±3/71±2mmHg). The baseline pulse rates were similar between the two groups. Blood pressure increased during tooth extraction in both groups; however, changes in blood pressure did not differ between them. Administration of local anesthetic significantly decreased the %HF in normotensive patients (before vs. after anesthesia; 22.3±2.4vs. 13.8±2.7%, p<0.05). In contrast, the LF/HF significantly decreased during the local anesthesia and tooth extraction in hypertensive patients. These results suggest that pressor response induced by tooth extraction did not differ between normotensive and hypertensive patients, and that suppression of the cardiac sympathetic nervous system during dental surgery might attenuate the pressor response in patients with hypertension. (Hypertens Res 2000; 23: 207-212)

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Central muscarinic receptors play an important role in the regulation of cardiac vagal nerve activity. We studied the inhibition of central muscarinic receptors and sympathetic nerve function in humans, since very little information is currently available on this subject. We examined the effects of graded doses of atropine (five doses, range 0.001 to 0.016mg/kg) on heart rate, arterial pressure, heart rate variability, and muscle sympathetic nerve activity in 13 healthy young volunteers. Atropine caused biphasic effects on heart rate and the high-frequency (HF) power of R-R interval variability. At lower doses (_??_0.002mg/kg for heart rate, 0.001mg/kg for HF power), atropine decreased heart rate and increased HF power. In contrast, at higher doses, atropine increased heart rate and decreased HF power. Low-dose atropine significantly attenuated muscle sympathetic nerve activity, burst rate (bursts/min) by -30.5±6.0% and burst incidence (bursts/100 heart beats) by -23.8±6.9% at 0.002mg/kg. Systolic and diastolic arterial pressure did not change with atropine infusion. Low-dose atropine (_??_0.002mg/kg) did not significantly affect either low frequency (LF) power or LF/HF. These results suggest that central muscarinic receptors may modulate not only cardiac vagal nerve activity but also sympathetic nerve activity in the skeletal muscle vasculature. (Hypertens Res 2000; 23: 213-218)

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It has been demonstrated that antihypertensive treatment of hypertensive diabetic patients is quite effective in preventing macrovascular and microvascular complications and improving prognosis. Nevertheless, the target blood pressure level of antihypertensive treatment in hypertensive diabetic patients with microalbuminuria (i.e., with early diabetic nephropathy) remains to be established. In this study, we evaluated the effect of intensive blood pressure control (diastolic blood pressure <80mmHg) on urinary albumin excretion in hypertensive, type II diabetic patients with microalbuminuria. We examined the effects of a combination therapy using an angiotensin-converting enzyme (ACE) inhibitor plus a long-acting calcium channel blocker (amlodipine), and compared them with the effect of an ACE inhibitor alone. Thirty hypertensive, type II diabetic patients with microalbuminuria were treated with either an ACE inhibitor alone (group I, n=17) or an ACE inhibitor plus amlodipine (group II, n=13) for 32 weeks. With treatment, blood pressures in both groups were significantly reduced, and diastolic blood pressure was lowered to a much greater extent in group II (76±2mmHg) than in group I (83±2mmHg, p<0.05). Although the urinary albumin excretion rate was decreased in both groups, the decrease attained statistical significance only in group II (from 141±25mg/day to 69±18mg/day, p<0.05); the extent of reduction in microalbuminuria during antihypertensive treatment was significantly greater in group II (50±10%) than in group I (14±13%, p< 0.05). In conclusion, this study showed that in hypertensive microalbuminuric type II diabetic patients, the combination of an ACE inhibitor plus amlodipine resulted in a more pronounced decreased in blood pressure (diastolic blood pressure <80mmHg) and a greater reduction in urinary albumin excretion than did use of an ACE inhibitor alone. This combination strategy should thus be a more effective tool for obtaining optimal blood pressure control in patients with diabetic nephropathy. (Hypertens Res 2000; 23: 219-226)

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The effects of belonging to sports clubs on male high school students was evaluated. The relationships between the type and extent of school-based exercise were examined in conjunction with percent body fat, blood pressure (BP), and other key metabolic parameters. A total of 264 male Japanese high school students (age range: 17-18 years old) were studied. Percent body fat was measured and blood was collected in the fasting state during a routine health check. Subjects were divided into two groups. The exercise (E) group (n=150) included students who had belonged to a sports club during the past 2 years. The non-exercise (NE) group (n=114) included students who did not belong to a sports club during the past 2 years. The body mass index was significantly greater in group E (21.7±2.3 (SD) kg/m²) than in group NE (20.7+ 2.6kg/m², p<0.01). However, the percent body fat in group E (13.6±3.4%) was significantly lower than that in group NE (14.9±3.8%, p<0.01). The diastolic BP and heart rate in group E (64±7mmHg, 70± 11/min) were significantly lower in group E than in group NE (66±8mmHg, p<0.05; 76±14/min, p< 0.01). The serum triglyceride level was significantly lower, and the HDL cholesterol level was higher in group E than in group NE. The homeostasis model assessment (HOMA) index, used as an index of insulin resistance, was similar in the two groups. However, the level of the HOMA index was significantly lower among the 62 subjects in group E who preferred highly dynamic exercise (1.50±0.46) than it was among those in group NE (1.66±0.49, p<0.05). Results indicate that belonging to sports clubs influences the BP and lipid profiles of adolescent males, as well as their percent body fat. In view of the reduction of cardiovascular risk factors, it is recommended that even young males practice regular exercise, especially aerobic exercise. (Hypertens Res 2000; 23: 227-232)

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Impaired endothelial function has been reported to be the initial step in atherosclerosis. Some coronary risk factors independently relate to impaired endothelial function. However, few studies have examined the association between coronary risk factors and endothelial function in patients who have multiple risk factors without clinical atherosclerosis. This study was undertaken to elucidate the relationship between accumulation of coronary risk factors and vascular endothelial dysfunction. We examined 101 subjects with one or more coronary risk factors 56.8±1.0 years old and 40 age-matched control subjects without coronary risk factors. We measured brachial artery diameter non-invasively using a 7.5-MHz ultrasound machine at rest, during reactive hyperemia caused by endothelium-dependent vasodilatation, and after sublingual administration of nitroglycerin, which causes endothelium-independent vasodilatation. The percentage change in flow-mediated diameter (%FMD; ΔD/D×100), in subjects with one or more coronary risk factors was significantly lower than that in control subjects (4.8±0.3% vs. 6.7±0.5% p<0.01). Endothelium-independent vasodilatation by nitroglycerin did not differ between the two groups. Endothelial function was impaired according to the accumulation of coronary risk factors. On multiple regression analysis, the number of risk factors, age, and brachial artery diameter at rest showed significant correlation with %FMD. Our results suggest that an accumulation of coronary risk factors was significantly related to impairment of endothelial function. (Hyperfens Res 2000; 23: 233-238)

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To elucidate the mechanism of left ventricular dysfunction associated with left ventricular hypertrophy in hypertension, coronary blood flow (CBF) and left ventricular mass (LVM) were measured in 62 patients with essential hypertension (mean age, 54±13 years) and 22 normotensive control subjects (mean age, 57 ±13 years). According to the indicator fractionation principle, CBF/cardiac output (CO), estimated on the basis of the ratio of myocardial uptake/total injected dose of thallium-201 (% cardiac uptake), was measured. CBF and CBF per 100g of myocardium (unit CBF) were calculated according to the following formulas: CBF=% cardiac uptake×CO, and unit CBF=(CBF/LVM)×100, where CO and LVM are echocardiographically determined. Midwall fractional shortening (FS) and isovolumic relaxation time (IRT) were calculated as the indices of systolic and diastolic functions. CBF was greater in hypertensives than in controls (218.2±74.0 vs. 187.4±40.4ml/min, p<0.05), though unit CBF was smaller in hypertensives than in controls (99.1±22.0 vs. 141.2±31.6ml/min/100g, p<0.0001). Multiple regression analyses showed that unit CBF was the most potent predictor of both midwall FS and IRT. A positive correlation was found between midwall FS and unit CBF (r=0.669, p<0.0001), and a negative correlation between IRT and unit CBF (r=-0.579, p<0.0001). In conclusion, myocardial ischemia reflected by the decrease in unit CBF may be closely related to left ventricular dysfunction in patients with essential hypertension. (Hypertens Res 2000; 23: 239-245)

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A 68-year-old woman was found to have atypical coarctation of the aorta, accompanied by systolic hypertension of the upper extremities despite administration of five types of antihypertensive drugs. Since the systolic hypertension was resistant to the conventional antihypertensive therapy, axilloiliac artery bypass grafting with a subcutaneous tunnel was performed to alleviate the pressure gradient. Systolic blood pressure was successfully reduced and hypertension was controlled after surgery. (Hypertens Res 2000; 23: 247-249)

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Angiotensin converting enzyme (ACE) inhibitors inhibit the degradation of bradykinin and contribute to accumulation of bradykinin and NO, both of which may be beneficial for diseased hearts. To test this idea, we administered imidaprilat and cilazaprilat, respectively to the canine ischemic myocardium. In the open chest dogs with low constant coronary perfusion pressure (CPP, from 104±3 to 42±3mmHg), coronary blood flow (CBF, 91±1 to 32±2ml/100g/min), fractional shortening (FS), and lactate extraction ratio (LER) decreased. Either imidaprilat or cilazaprilat increased CBF, FS, and LER with increases in cardiac bradykinin and NO levels. The beneficial effects of ACE inhibitors were blunted by either L-NAME (an inhibitor of NO synthase) and HOE140 (an inhibitor of bradykinin receptors), respectively. ACE inhibitors, on the other hand, are reported to attenuate the severity of myocardial stunning, which effect is partially attributable to bradykinin- and NO-dependent mechanisms. Further, ACE inhibitors limited infarct size following coronary occlusion and reperfusion. This infarct size-limitation was blunted by either L-NAME and IBTX (the antagonist of K_Ca channels). Bradykinin is also reported to close K_Ca channels. Thus, we concluded that ACE inhibitors attenuate both reversible and irreversible myocardial cellular injury via bradykinin/NO-dependent mechanisms. In experimental and clinical settings, the cardioprotective effects of ACE inhibitors on the diseased heart may be attributable to these mechanisms. (Hypertens Res 2000; 23: 253-259)

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To investigate the correlation of polymorphism of angiotensin-converting enzyme (ACE) genes with left ventricular hypertrophy in essential hypertension, 151 patients with essential hypertension were studied. ACE genotypes were determined by PCR technology and diastolic left ventricular diameter (DLVd), systolic left ventricular diameter (SLVd), interseptal ventricular thickness (IVS), and left ventricular posterior wall thickness (LVPW) were scanned by echocardiography. Left ventricular mass (LVM) and the left ventricular mass index (LVMI) were calculated from echocardiographic findings. Results revealed that DLVd, SLVd, IVS, LVPW, LVM, and LVMI of the DD genotype group were 49.9±5.6mm, 30.5±6.5mm, 11.2±1.6mm, 11.7±1.5mm, 259.5±62.1g, 92.7±23.5g/m², respectively. DLVd, SLVd, IVS, LVPW, LVM, and LVMI of the ID genotype group were 8.9±5.3mm, 31.5±5.2mm, 11.4±1.7mm, 11.9±1.6mm, 261.3±70.3g, and 94.9±25.8g/m², respectively, and DLVd, SLVd, IVS, LVPW, LVM, and LVMI of the II genotype group are 48.9±5.5mm, 31.8±6.5mm, 11.1±1.9mm, 11.5±1.8mm, 250.8±82.5g and 90.8±30.1g/m² respectively. There was no significant difference between the ID, DD and II genotype groups as regards DLVd, SLVd, IVS, LVPW, LVM, and LVMI (p>0.05). These findings indicate that there is no association between the ACE gene and left ventricular hypertrophy in essential hypertension occurring in the Chinese population. (Hypertens Res 2000; 23: 261-264)

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Essential Hypertension (EH) is correlated with a metabolic disturbance characterized by insulin resistance (IR). In this study, there were observed in 47 subjects with EH and 30 subjects with normal blood pressure. Serum levels of insulin-like growth factor-1 (IGF-1), serum levels of growth hormone (GH), the activity of erythrocyte insulin receptors (EIR), and ATP levels in erythrocytes, the insulin sensitivity index (ISI) was used to study the correlative factors of essential hypertension. 1. Among patients with EH, ISI, GH, and low-affinity insulin binding sites of EIRs (RT₂) were found to be in significantly lower amounts, IGF-1 levels and the KD₂ of the erythrocyte insulin receptors were noted to be significantly higher. Compared with the control group, there was a marked difference between EH group and the control group. However, no statistical difference was observed between the hypertensive group and the group with normal blood pressure as regards erythrocyte ATP levels, high-affinity insulin binding sites of EIRs (RT₁), and the KD₁ of EIRs. 2. In the hypertensive group, the ISI was negatively correlated with mean arterial blood pressure (MBP), a family history of hypertension, the body mass index (BMI), the waist-hip ratio (WHR) and IGF-1 levels (r=-0.614^Δ, -0.354^**, -0.386^**, -0.472^**, -0.298^*, ^Δp<0.001, ^**p<0.01, ^*p<0.05), were positively correlated with RT₂ and GH levels (r=0.301^**, 0.275^*, ^**p<0.01, ^*p<0.05). There were no statistically significant differences between ISI and age, sex, smoking history, drinking, RT₁, KD₁, and ATP levels in erythrocytes. 3. The ISI was used as the dependent variable in multiple linear stepwise regression analysis. MBP (X₁), a family history of EH (X₂), WHR (X₃), GH (X₄), IGF-1 (X₅), RT₂ (X₆), and the body mass index (X₇) was used as independent variables. X₁, X₂, X₃, X₅, X₆, and X₇ were used in the equations. The results indicate that patients with EH also tend to have IR. We suggest that MBP, a family history of hypertension, BMI, WHR, IGF-1, and RT₂ might be independent factors affecting IR in cases of essential hypertension. (Hypertens Res 2000; 23: 265-270)

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The ε4 allele of apolipoprotein E (APOE) is reported to be a genetic risk factor of atherosclerosis through hyperlipidemia and late-onset Alzheimer's dementia. A recent report showed that a genetic variant (A -491T) in the promoter region of the APOE gene increases the risk of Alzheimer's disease. In the present study, we examined whether these APOE polymorphisms were genetically involved in essential hypertension. Japanese hypertensives (n=180) with a family history of hypertension and normotensive controls (n =195, sex and age matched with hypertensives) were recruited from the outpatients of Osaka University Hospital, and an informed consent to participate in the study was obtained from each person. APOE polymorphisms were determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The frequencies of the A -491 allele in hypertensives and normotensives were 0.98 and 0.97, respectively, and the TT/-491 genotype was not found in either group. No significant differences between hypertensives and normotensives were observed in allele frequencies in either APOE polymorphism; however, the mean diastolic blood pressure in normotensive subjects with AA/-491 was significantly higher than in the subjects with AT/-491 (p<0.01). These results suggest that the presence of the APOE promoter polymorphism is not a major risk factor for hypertension but that it does have some minor effect on basal blood pressure variation. (Hypertens Res 2000; 23: 271-275)

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

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Oxidative stress has been reported to be involved in not only cardiovascular diseases but in hypertension, which is a major risk for cardiovascular diseases. Urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) has been recognized as a sensitive biomarker of oxidative DNA damage and also of oxidative stress. In the present study, we assessed the oxidative stress in human subjects with hypertension and in hypertensive rats. In stroke-prone spontaneously hypertensive rats at the age of 14 weeks, the excretion of urinary 8-OHdG was significantly (p<0.05) increased compared with that in age-matched normotensive Wistar-Kyoto rats. Next, we investigated the relationship between oxidative DNA damage and cardiovascular risk factors among Tanzanians aged 46-58 years in a population study carried out in 1998 in at Dar es Salaam, Tanzania, according to the WHO-CARDIAC Study Protocol. Sixty subjects (male/female, 28/32) were selected by SPSS Base 8.0 from those who completed a 24-h urine collection. The 24-h urinary 8-OHdG of the hypertensive subjects (SBP_??_140mmHg and/or DBP_??_90mmHg) was significantly (p<0.05) higher than that of the normotensive subjects (SBP<140mmHg and DBP<90mmHg) after adjusting for age and gender (Hypertensives: 17.31±2.0ng/mg creatinine, n=38; Normotensives:10.10±2.64ng/mg creatinine, n=22). Oxidative stress was thought to be involved in hypertensive subjects and in hypertensive rats. (Hypertens Res 2000; 23: 285-289)

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