Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1996;27:408-413

This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kawamura, M.
Right arrow Articles by Hiramori, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kawamura, M.
Right arrow Articles by Hiramori, K.

(Hypertension. 1996;27:408-413.)
© 1996 American Heart Association, Inc.


Articles

Factors That Affect Calorie-Sensitive and Calorie-Insensitive Reduction in Blood Pressure During Short-term Calorie Restriction in Overweight Hypertensive Women

Minoru Kawamura; Toshiyuki Adachi; Jun Nakajima; Takuya Fujiwara; Katsuhiko Hiramori

From the Second Department of Internal Medicine, Iwate Medical University, Morioka, Japan.

Correspondence to Minoru Kawamura, MD, Second Department of Internal Medicine, Iwate Medical University, Uchimaru 19-1, Morioka, Iwate, 020 Japan.


*    Abstract
up arrowTop
*Abstract
down arrowIntroduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Abstract This study was performed to elucidate the factors that affect the reduction in blood pressure produced by calorie restriction in overweight women with essential hypertension. Fifty-one subjects were admitted to the metabolic ward of the hospital. After being fed a standard diet (6.3 to 8.4 MJ/d) for 2 weeks, the calorie-restricted group (n=34) was fed a low-calorie diet (1.9 MJ/d) for an additional 2 weeks. The calorie-nonrestricted group (n=17) was fed the standard diet for 4 weeks. Sodium and potassium intake was kept constant, as was the level of exercise activity. The calorie-restricted group was subdivided into "calorie-sensitive" and "calorie-insensitive" groups based on an average 5 mm Hg reduction in mean blood pressure during the low-calorie diet. The mean age was 51±6 years (mean±SD) in the calorie-sensitive group (n=16), which was significantly lower than the mean age of 61±6 years in the calorie-insensitive group (n=18). Multiple regression analysis indicated that age and change in body weight exhibited significant correlations with blood pressure reduction produced by calorie restriction among 17 parameters. Findings suggest that age can predict the extent of blood pressure reduction that would be obtained during 2 weeks of calorie restriction in overweight hypertensive women. The reduction in blood pressure may be related in part to the amount of weight loss.


Key Words: hypertension, essential • weight loss • calorie restriction • low-calorie diet • age • sodium balance


*    Introduction
up arrowTop
up arrowAbstract
*Introduction
down arrowMethods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Extensive studies1 2 have demonstrated an association between the overweight condition and hypertension. Prospective trials demonstrate that blood pressure is reduced by weight loss.3 Recent studies4 5 6 7 8 9 10 suggest that the blood pressure of hypertensive, overweight patients is reduced by calorie restriction during a constant intake of sodium. However, only limited information is available about the hypotensive mechanism involved. A decrease in sympathetic nervous system activity,11 suppression of the renin-angiotensin system,12 and suppression of insulin secretion13 have all been suggested as possible mechanisms of blood pressure reduction in patients who range over a spectrum of normotension to moderate hypertension. A decrease in sympathetic nervous system activity has been suggested to be the mechanism for the blood pressure reduction in overweight patients with hypertension who were placed on a low-calorie diet.9 However, since these studies did not use calorie-nonrestricted patients as control subjects, many factors that affect blood pressure besides caloric intake may be involved, including a change in environmental factors,14 physical activity,15 and acclimation to blood pressure measurement.16 We recently found in a randomized, 2-week controlled study that a calorie-restricted group experienced a significantly greater reduction in blood pressure than the control subjects under a constant intake of dietary sodium and potassium and physical activity.17 This strongly suggests that calorie restriction alone can rapidly reduce blood pressure. The extent of reduction obtained varies, which suggests that individuals may be calorie sensitive or calorie insensitive. However, the factors or mechanisms responsible for such "calorie sensitivity" remain to be elucidated.

We evaluated factors that affected the reduction in blood pressure produced by calorie restriction in calorie-restricted versus calorie-nonrestricted groups and also between calorie-sensitive versus calorie-insensitive groups while controlling for other dietary variables and physical activity. Changes in blood pressure were examined relative to baselines and changes in neuroendocrine and electrolyte parameters.


*    Methods
up arrowTop
up arrowAbstract
up arrowIntroduction
*Methods
down arrowResults
down arrowDiscussion
down arrowReferences
 
Patients
We evaluated 57 Japanese women 40 to 70 years old with essential hypertension who were overweight (body weight, 50 to 80 kg; body mass index, 25 to 30 kg/m2). They were postmenopausal or had undergone hysterectomy for myomas, so that uninterrupted daily urine collection was feasible. To be admitted to the study, they were required to exhibit a systolic blood pressure >160 mm Hg and/or a diastolic blood pressure >95 mm Hg on at least three separate occasions in the absence of treatment or during treatment with antihypertensive medication. A complete medical workup was performed within 1 week of admission to exclude secondary forms of hypertension. Renal function was judged to be normal on the basis of normal serum creatinine, normal intravenous pyelography, and absence of proteinuria. Patients were categorized as stage 1 or stage 2 hypertensive according to World Health Organization classification. Antihypertensive agents were withdrawn 2 weeks before admission to the study and were withheld until the end of the study. This investigation was approved by the Ethical Supervisory Committee of Iwate Medical University. All subjects were provided with detailed information about the protocol and gave informed consent before participation.

Procedures
The 57 women were admitted to the metabolic ward of the Iwate Medical University Hospital for this 4-week study. They were assigned on study entry to either a calorie-restricted group or a calorie-nonrestricted group. After being fed a standard diet (6.3 to 8.4 MJ/d) for 2 week (weeks 1 and 2), the calorie-restricted group was fed a low-calorie diet consisting of Optifast (Sandoz Nutrition) and vegetables for an additional 2 weeks (weeks 3 and 4). The calorie-nonrestricted group was fed the standard diet for 4 weeks (weeks 1 through 4). Strenuous exertion was prohibited during this period, and the extent of exercise (walking) was measured with a pedometer (HJ-7, Omron Inc). Subjects were asked to walk a constant distance ranging from 4000 to 8000 steps per day, as determined by individual exercise capacity. They recorded the number of steps walked each day in a diary. They were also asked to drink a constant daily volume of water ranging from 1.0 to 1.5 L in addition to eating their meals during the study. Patients who complained of constipation during the study received cathartics. Three patients were discharged before the end of the study because of unexpected business commitments, and 3 patients discontinued the protocol because they disliked the taste of Optifast. These 6 patients were subsequently excluded from evaluation. Ultimately, 51 patients completed the protocol, and their data were evaluated. Before entry, antihypertensive drugs were administered to 41 patients, and the remaining 10 patients received no antihypertensive medication. A calcium channel blocker was administered to 28 patients, an angiotensin-converting enzyme inhibitor to 11 patients, a diuretic to 4 patients, and a ß-blocker to 3 patients (one drug was administered to 36 patients, and two drugs were administered to 5 patients).

Diet
Except for potassium content, constituents of the standard diet and the vegetables added in the low-calorie diet were determined from standard tables.18 Constituents of Optifast were determined from the manufacturer's manual. The potassium content of the standard diet and vegetables added in the low-calorie diet was obtained from measurements using a method of food digestion.10 In our previous reports,10 17 sodium intake in the standard diet varied widely day to day (coefficient of variation, 0.23) because of the addition of salt during cooking. In the present study, to maintain a constant sodium intake, the standard diet contained no added sodium chloride. The daily standard diet contained either 6.3, 7.1, or 8.4 MJ, with 85 to 90 g protein, 45 to 60 g fat, 180 to 275 g carbohydrates, 30 to 50 mmol sodium, and 40 to 60 mmol potassium. Each patient selected one of the three different amounts of calorie intake within 7 days of admission, although we recommended the amount of calorie intake as judged from the body weight, age, and exercise activity of the individual patient. The daily low-calorie diet consisted of Optifast and vegetables containing 1.9 MJ, with 70 g protein, 2 g fat, 35 g carbohydrates, 40 mmol sodium, and 60 mmol potassium. Each diet contained equal amounts of sodium (120 mmol) and potassium (60 mmol) per day, since the standard diet was supplemented with 80 mmol sodium (NaCl) and 8 mmol potassium (Slow K, Japan Ciba Geigy Pharmaceuticals) and the low-calorie diet with 80 mmol sodium to equalize the mineral content. All patients received 859±41 mmol sodium per week in the standard diet and 847±9 mmol per week in the low-calorie diet. The week-to-week coefficients of variation were 0.05 and 0.01, respectively. The amount of calcium in each diet was 20 to 30 mmol per day.

Measurements and Calculations
Blood samples were collected at 7 AM after the patients had rested 30 minutes in the supine position on day 3 or 4 of each week of study. On each day of the study, 24-hour urine was collected, blood pressure was measured, and body weight was determined. The nursing staff measured the blood pressure and pulse rate on the same arm with a standard mercury sphygmomanometer at 6 AM, 10 AM, 2 PM, and 6 PM after the patients had rested 10 minutes in the supine position. The staff was well trained in measuring blood pressure. The diastolic pressure was taken as the level at which the Korotkoff sounds disappeared. The mean blood pressure was calculated by adding one third of the pulse pressure to the diastolic pressure. The pulse rate was counted for 1 minute after the blood pressure had been measured; blood was then drawn. Body weight was measured on an electronic strain-gauge scale (EDI-303H, Yamato Co, Ltd) at 6:30 AM after voiding; the value recorded was considered the body weight for the previous day. Blood pressure, pulse rate, and body weight were expressed as average values of 7 days in each week. The 24-hour urine collection was done between 7 AM and 7 AM at 4°C. Each urine sample was poured into an apparatus that divided the urine into two equal portions. Concentrated hydrochloric acid was added to one portion to measure norepinephrine. One fiftieth of each portion was stored at -20°C. The samples obtained during each week were thawed, mixed together, and then measured. Urinary norepinephrine was estimated by high-speed ion-exchange chromatography and the trihydroxyindole method.19 Serum and urinary sodium concentrations were measured by flame photometry. Urinary C peptide levels were determined by radioimmunoassay using a commercial kit (Shionogi Laboratory). Serum acetoacetate levels were estimated according to the method of Harano et al20 with a commercial kit (Sanwakagaku Laboratory).

Statistical Methods
Values are expressed as mean±SD. Significance of the differences between the calorie-restricted and calorie-nonrestricted groups, between the calorie-sensitive and calorie-insensitive groups, and between the calorie-insensitive and calorie-nonrestricted groups were determined by the Mann-Whitney test. Taking change in mean blood pressure produced by calorie restriction as the dependent variable and 17 parameters as independent variables, we performed multiple regression analysis. A level of P<.05 was accepted as statistically significant.


*    Results
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
*Results
down arrowDiscussion
down arrowReferences
 
There were no significant differences between the calorie-restricted group (n=34) and the calorie-nonrestricted group (n=17) in mean values for age (56±7 versus 57±8 years), body weight (66.6±6.6 versus 65.3±7.0 kg), body mass index (28.5±2.7 versus 29.0±3.0 kg/m2), calorie intake (7.5±0.9 versus 7.4±1.0 MJ/d), systolic/diastolic blood pressures (147±15/90±7 versus 149±10/91±6 mm Hg), urinary norepinephrine (4.11±1.32 versus 3.76±0.87 µmol/wk), C peptide (108±50 versus 105±40 nmol/wk) and sodium (700±77 versus 686±62 mmol/wk) excretions, and other parameters measured (data not shown) during week 2. Table 1Down indicates changes from week 2 to weeks 3 and 4 between the two groups. The calorie-restricted group experienced a significant reduction in systolic and diastolic blood pressures with weight loss, elevated sodium excretion, and acetoacetate concentration and reduced norepinephrine and C peptide excretions compared with the calorie-nonrestricted group.


View this table:
[in this window]
[in a new window]
 
Table 1. Comparison of Changes From Week 2 (Baseline) vs Weeks 3 and 4 Between Calorie-Restricted and Calorie-Nonrestricted Groups

The average reduction in mean blood pressure during weeks 3 and 4 in the calorie-nonrestricted group was 1.0±2.0 mm Hg, and the 95% confidence interval was a range of -3 to 5 mm Hg. Therefore, the calorie-restricted group was subdivided into calorie-sensitive and calorie-insensitive groups, with a criterion of 5 mm Hg of reduction in mean blood pressure during weeks 3 and 4. Sixteen patients belonged to the calorie-sensitive subgroup and 18 patients belonged to the calorie-insensitive subgroup. The FigureDown shows changes in mean blood pressure from week 2 to weeks 3 and 4. The calorie-sensitive group experienced a significantly greater reduction in blood pressure than did the calorie-insensitive and calorie-nonrestricted groups, and no significant difference was observed in the reduction between the calorie-insensitive and calorie-nonrestricted groups.



View larger version (18K):
[in this window]
[in a new window]
 
Figure 1. Comparative reduction in mean blood pressure in calorie-sensitive (dark hatched bars), calorie-insensitive (light hatched bars), and calorie-nonrestricted (shaded bars) groups during calorie restriction calculated by subtraction from baseline (week 2) to week 3 or 4. Values are mean±SD. *P<.001 versus calorie-sensitive group in week 3; {dagger}P<.001 versus calorie-sensitive group in week 4.

Table 2Down indicates no significant differences between the calorie-sensitive and calorie-insensitive groups for any parameter except age. In the calorie-sensitive group, 4 patients had undergone hysterectomy at the ages of 35, 38, 39, and 43 years, respectively; in the calorie-insensitive group, 3 patients had undergone hysterectomy at the ages of 39, 40, and 46 years, respectively. Except for these 7 women, there was no significant difference in the age of menopause (50±2 versus 50±3 years) between the two groups. Twelve patients (75%) in the calorie-sensitive group and 15 patients (83%) in the calorie-insensitive group had received antihypertensive drug(s) before entry.


View this table:
[in this window]
[in a new window]
 
Table 2. Comparison of Findings in Calorie-Sensitive vs Calorie-Insensitive Groups at Week 2 (Baseline)

Table 3Down indicates changes between week 2 and weeks 3 and 4 in the calorie-sensitive and calorie-insensitive groups. The calorie-sensitive group lost more weight and evidenced higher serum levels of acetoacetate than did the calorie-insensitive group during weeks 3 and 4. Norepinephrine and C peptide excretion did not differ between the two groups.


View this table:
[in this window]
[in a new window]
 
Table 3. Comparison of Changes From Week 2 (Baseline) vs Weeks 3 and 4 Between the Calorie-Sensitive and Calorie-Insensitive Groups

To evaluate the reduction in blood pressure produced by calorie restriction and any relation to any other variables, multiple regression analysis was performed in the calorie-restricted group. With change in mean blood pressures taken as the dependent variable and 17 parameters as independent variables, age and change in body weight exhibited significant inverse correlations with blood pressure reduction (Table 4Down).


View this table:
[in this window]
[in a new window]
 
Table 4. Multiple Regression Analysis of Factors Related to Reduction in Blood Pressure


*    Discussion
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
Results of the present study confirmed that after 2 weeks on the regimen, the calorie-restricted group of overweight, hypertensive women experienced a significantly greater reduction in blood pressure than those given unrestricted calories. The results of this carefully designed and implemented study suggest that calorie restriction lowered blood pressure independently of the intake of sodium, potassium, or calcium and of exercise (walking). This observation corresponds with findings of recent studies4 5 6 7 8 9 10 except for those reported by Andersson et al21 in overweight patients with hypertension.

To the best of our knowledge, this is the first report to find age to be a predictive factor in the reduction of blood pressure produced by calorie restriction over a constant period of time in overweight women with hypertension. Although reduction in the body weight of overweight hypertensive patients is a recommended lifestyle modification,22 23 poor compliance is a major problem.24 The present finding may be especially useful in encouraging younger overweight patients with hypertension to undergo weight reduction.

The reduction of blood pressure produced by calorie restriction can be explained in part by differences in the amount of weight lost. Several long-term studies5 25 26 27 indicate a statistically significant difference between the reduction in body weight attained by calorie restriction and the reduction in blood pressure. Staessen et al,28 who conducted a meta-analysis of 11 studies reported between 1954 and 1985, estimated that the effect of a 1-kg reduction in body weight was a reduction of 1.6 mm Hg in systolic blood pressure and 1.3 mm Hg in diastolic blood pressure. Our study resulted in similar values: reductions of 2.5 mm Hg in systolic blood pressure and 1.3 mm Hg in diastolic blood pressure.

What mechanisms are involved in the reduction in blood pressure produced by calorie restriction? Sympathetic nervous system activity and/or insulin secretion are thought to be involved in the renal and cardiovascular mechanisms of hypertension in obesity.29 Judging from the present data on urinary excretions of norepinephrine and C peptide showing no differences in these substances between the calorie-sensitive and calorie-insensitive groups (Table 3Up) and no significant correlations between these substances and reduction in blood pressure (Table 4Up), there was no indication that sympathetic nervous system activity or insulin secretion was involved in a lowering of blood pressure. These changes could merely reflect calorie restriction, since significant differences in urinary excretion of norepinephrine and C peptide were observed between the calorie-restricted and calorie-nonrestricted groups (Table 1Up). This corresponds to the results of a study by Weinsier et al8 that evaluated the separate effects of energy restriction and weight reduction, but it is inconsistent with the findings of Kushiro et al9 that the change in blood pressure was correlated with the percent change in norepinephrine during calorie restriction in overweight, hypertensive patients. The change in blood pressure in that study may have been due, at least in part, to the spontaneous reduction related to hospitalization, since the blood pressure of patients with essential hypertension often decreases upon admission to the hospital, especially in the initial week.14 Subjects in their study were switched to a low-calorie diet on day 6 after admission.

The lack of difference in the urinary excretion of norepinephrine between the calorie-sensitive and calorie-insensitive groups may be explained by a possible problem in the method used to estimate sympathetic nervous system activity. Urinary norepinephrine excretion presents an indirect index of sympathetic nervous system activity, since a considerable amount of the norepinephrine released is taken up again.30 The role of sympathetic nervous system activity in such patients should be evaluated by a microneurographic technique that allows the direct measurement of sympathetic neural discharge in humans.31

The renin-angiotensin system is also thought to be involved in the weight-related changes in blood pressure.12 The present controlled study indicated no statistically significant difference in the change in renin activity during calorie restriction between the calorie-sensitive and calorie-insensitive groups (Table 3Up). The absolute renin activities were comparatively low (Table 2Up), suggesting that the renin-angiotensin system may not be involved in the hypotensive mechanism of calorie restriction over the short term, although the role of the tissue renin-angiotensin system32 remains to be elucidated.

The present study indicated a negative sodium balance during calorie restriction (Table 1Up), as previously reported by Weinsier et al.8 Although a low-sodium diet produces a negative sodium balance33 and thus probably plays some role in the reduction of blood pressure, the hypotensive response to diuretic administration is unrelated to the extent of the negative sodium balance.34 We observed no difference in the quantitative balance between the calorie-sensitive and calorie-insensitive groups (Table 2Up) and no correlation between the quantitative balance and the blood pressure reduction (Table 4Up), which suggests that the hypotensive response to calorie restriction is unrelated to the extent of negative sodium balance, an idea that corresponds with previous reports.8 10

Thus, although in the present study blood pressure was found to be reduced by calorie restriction, neurohormonal data did not explain the mechanism. It is possible that the release of other vasoactive substances, including endothelium-derived relaxing factors and atrial natriuretic peptide, is involved. Alternatively, differences in vascular reactivity may be involved in the differences in changes in blood pressure through aging, because aging is associated with changes in the structure and function of the arteries35 ; the vascular responses of endothelium-derived relaxing factors36 and atrial natriuretic peptide37 are all reduced with age. In addition, differences in vascular reactivity may reflect the changes in the structure and function of arteries caused by hypertension, although whether endothelium-dependent relaxation is diminished in hypertensive patients remains controversial.38

We found no difference between the calorie-sensitive and calorie-insensitive groups in menopausal age, which corresponded to average menopausal age in Japanese women.39 In both groups, {approx}80% of patients had taken antihypertensive drugs before the study, most commonly a calcium channel blocker. It is therefore unlikely that these two factors influenced the results between the calorie-sensitive and calorie-insensitive groups.

We emphasize that the present study involved a short period of severe calorie restriction and that we excluded patients with organ damage from the study. Accordingly, the effect of prolonged, mild calorie restriction as well as the effects of organ damage on the reduction in blood pressure achieved on a restricted diet remain to be elucidated.

In summary, our results suggest that age was a predictor of the extent of blood pressure reduction during 2 weeks of marked calorie restriction in overweight, hypertensive women. The reduction in blood pressure may be related in part to the amount of weight loss.


*    Acknowledgments
 
This work was supported by a Research Grant for Cardiovascular Diseases (3C-5) from the Ministry of Health and Welfare of Japan.

Received May 16, 1995; first decision June 30, 1995; accepted November 24, 1995.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 
1. Kannel WB, Brand N, Skinner JJ Jr, Dawber TR, McNamara PM. The relation of adiposity to blood pressure and development of hypertension. Ann Intern Med. 1967;67:48-59.

2. Stamler R, Stamler J, Riedlinger WF, Algera G, Roberts RJ. Weight and blood pressure: findings in hypertension screening of one million Americans. JAMA. 1978;240:1607-1610. [Abstract/Free Full Text]

3. Berchtold P, Jorgens V, Kemmer FW, Berger M. Obesity and hypertension: cardiovascular response to weight reduction. Hypertension. 1982;4(suppl III):III-50-III-55.

4. Reisin E, Abel R, Modan M. Effect of weight loss without salt restriction on the reduction of blood pressure in overweight hypertensive patients. N Engl J Med. 1978;298:1-6.

5. Reisin E, Frohlich ED, Messerli FH, Dreslinski GR, Dunn FG, Jones MM, Batson HM Jr. Cardiovascular changes after weight reduction in obesity hypertension. Ann Intern Med. 1983;98:315-319.

6. Gillum RF, Prineas RJ, Jeffery RW, Jacobs DR, Elmer PJ, Gomez O. Nonpharmacologic therapy of hypertension: the independent effects of weight reduction and sodium restriction in overweight borderline hypertensive patients. Am Heart J. 1983;105:128-133. [Medline] [Order article via Infotrieve]

7. Morton H, Maxwell MH, Kushiro T, Dornfeld LP, Tuck ML, Waks AU. BP changes in obese hypertensive subjects during rapid weight loss. Arch Intern Med. 1984;144:1581-1584. [Abstract/Free Full Text]

8. Weinsier RL, James LD, Darnell BE, Dustan HP, Birch R, Hunter GR. Obesity-related hypertension: evaluation of the separate effects of energy restriction and weight reduction on hemodynamic and neuroendocrine status. Am J Med. 1991;90:460-468. [Medline] [Order article via Infotrieve]

9. Kushiro T, Kobayashi F, Osada H, Tomiyama H, Satoh K, Otsuka Y, Kurumatani H, Kajiwara N. Role of sympathetic activity in blood pressure reduction with low calorie regimen. Hypertension. 1991;17:965-968. [Abstract/Free Full Text]

10. Kawamura M, Kojima S, Akasaka T, Kasatsuki T, Hiramori K, Ito K, Omae T. Effect of a hypocaloric diet on blood pressure and sodium balance in overweight patients with essential hypertension. Hypertens Res. 1992;15:137-142.

11. Tuck ML, Sowers JR, Dornfeld L, Whitfield L, Maxwell M. Reductions in plasma catecholamines and blood pressure during weight loss in obese subjects. Acta Endocrinol. 1983;102:252-257.

12. Tuck ML, Sowers J, Dornfeld L, Kledzik G, Maxwell M. The effect of weight reduction on blood pressure, plasma renin activity and plasma aldosterone levels in obese patients. N Engl J Med. 1981;304:930-933. [Abstract]

13. Rocchini AP, Katch V, Schork A, Kelch RP. Insulin and blood pressure during weight loss in obese adolescents. Hypertension. 1987;10:267-273. [Abstract/Free Full Text]

14. Nishimura H, Nishioka A, Kubo S, Suwa M, Kino M, Kawamura K. Multifactorial evaluation of blood pressure fall upon hospitalization in essential hypertensive patients. Clin Sci. 1987;73:135-141. [Medline] [Order article via Infotrieve]

15. Rowlands DB, Stallard TJ, Watson RDS, Littler WA. The influence of physical activity on arterial pressure during ambulatory recording in man. Clin Sci. 1980;58:115-117. [Medline] [Order article via Infotrieve]

16. Watson RDS, Lumb R, Young MA, Stallard TJ, Davies P, Littler WA. Variation in cuff blood pressure in untreated outpatients with mild hypertension: implications for initiating antihypertensive treatment. J Hypertens. 1987;5:207-211. [Medline] [Order article via Infotrieve]

17. Kawamura M, Akasaka T, Kasatsuki T, Nakajinia J, Onodera S, Fujiwara T. Blood pressure is reduced by short-time calorie restriction in overweight hypertensive women with a constant intake of sodium and potassium. J Hypertens. 1993;11(suppl 5):S320-S321.

18. Resources Council of Agency of Science and Technology, Japan. Standard Tables of Food Composition in Japan. 4th ed. Resources Council Report. Tokyo, Japan: Ministry of Finance of Japan; 1982.

19. Mori K. High-speed ion-exchange chromatographic assay in the picomole range of biogenic amines. Ind Health. 1974;12:171-174.

20. Harano Y, Ohtsuki M, Ida M, Kojima H, Harada M, Okanishi T, Kashiwagi A, Ochi Y, Uno S, Shigeta Y. Direct automated assay method for serum or urine levels of ketone bodies. Clin Chim Acta. 1985;151:177-183. [Medline] [Order article via Infotrieve]

21. Andersson OK, Fagerberg B, Hedner T. Importance of dietary salt in the hemodynamic adjustment to weight reduction in obese hypertensive men. Hypertension. 1984;6:814-819. [Abstract/Free Full Text]

22. Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC V). The fifth report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med. 1993;153:154-183. [Abstract/Free Full Text]

23. World Hypertension League. Nonpharmacological interventions as an adjunct to the pharmacological treatment of hypertension: a statement by WHL. J Hum Hypertens. 1993;7:159-164. [Medline] [Order article via Infotrieve]

24. Dwyer JT. Treatment of obesity: conventional programs and fad diets. In: Bjorntorp P, Brodoff NB, eds. Obesity. Philadelphia, Pa: JB Lippincott Co; 1992:662-676.

25. Stokholm KH, Nielsen PE, Quaade F, Members of the Danish Obesity Project. Correlation between initial blood pressure and blood pressure decrease after weight loss. Int J Obes. 1982;6:307-312. [Medline] [Order article via Infotrieve]

26. Dornfeld LP, Maxwell MH, Waks AU, Schroth P, Tuck ML. Obesity and hypertension: long-term effects of weight reduction on blood pressure. Int J Obes. 1985;9:381-389. [Medline] [Order article via Infotrieve]

27. Cohen N, Flamenbaum W. Obesity and hypertension: demonstration of a `floor effect.' Am J Med. 1986;80:177-181. [Medline] [Order article via Infotrieve]

28. Staessen J, Fagard R, Lijnen P, Amery A. Body weight, sodium intake and blood pressure. J Hypertens. 1989;7(suppl 1):S19-S23.

29. Hall JE. Renal and cardiovascular mechanisms of hypertension in obesity. Hypertension. 1994;23:381-394. [Abstract/Free Full Text]

30. Esler MD, Hasking GJ, Willett IR, Leonard PN, Jennings GL. Noradrenaline release and sympathetic nervous system activity. J Hypertens. 1985;3:117-129. [Medline] [Order article via Infotrieve]

31. Grassi G, Seravalle G, Cattaneo BR, Bolla GB, Lanfranchi A, Colombo M, Giannattasio C, Brunani A, Cavagnini F, Mancia G. Sympathetic activation in obese normotensive subjects. Hypertension. 1995;25(part 1):560-563.

32. Inagami T, Mizuno K, Nakamaru M, Pandey K, Naruse M, Naruse K, Misono K, Okamura T, Kawamura M, Higashimori K. The renin-angiotensin system: an overview of its intracellular function. Cardiovasc Drugs Ther. 1988;2:453-458. [Medline] [Order article via Infotrieve]

33. Straus MB, Lamdin E, Smith WP, Bleifer DJ. Surfeit and deficit of sodium. Arch Intern Med. 1958;102:527-536. [Abstract/Free Full Text]

34. Leth A, Ibsen H. Changes in the ratio of plasma to interstitial fluid volume during long-term antihypertensive therapy. J Lab Clin Med. 1976;87:781-791. [Medline] [Order article via Infotrieve]

35. Wadsworth RM. Calcium and vascular reactivity in ageing and hypertension. J Hypertens. 1990;8:975-983. [Medline] [Order article via Infotrieve]

36. Taddei S, Virdis A, Mattei P, Ghiadoni L, Gennari A, Fasolo GB, Sudano I, Salvetti A. Aging and endothelial function in normotensive subjects and patients with essential hypertension. Circulation. 1995;91:1981-1987. [Abstract/Free Full Text]

37. Jansen TLTA, Smits P, Tan ACITL, Thien T. Attenuated forearm vasodilator response to atrial natriuretic factor in the elderly. Hypertension. 1991;18:640-647. [Abstract/Free Full Text]

38. Cockgroft JR, Chowienczyk PJ, Benjamin N, Ritter JM. Preserved endothelium-dependent vasodilatation in patients with essential hypertension. N Engl J Med. 1994;330:1036-1040. [Abstract/Free Full Text]

39. Kato I, Tominaga S, Suzuki T. Factors related to late menopause and early menarche as risk factors for breast cancer. Jpn J Cancer Res. 1988;79:165-172.[Medline] [Order article via Infotrieve]





This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kawamura, M.
Right arrow Articles by Hiramori, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kawamura, M.
Right arrow Articles by Hiramori, K.