长期补钙对儿单血压的影响

５５名４－５岁健康儿童分两组进行长期口服补钙的自身交叉对比试验，结果显示两组儿童补钙前后各自的平均２４ｈ尿钙排泄量均无显著变化，未提高补钙对儿童血压影响的证据。本研究提示尿钠、钠／钾的增加对血压水平的升高有显著影响。     

长期补钾补钙对盐敏感儿童血压及其尿钠代谢的影响

为观察长期适量补充钾盐及钙盐对盐敏感儿童血压及其尿钠代谢的影响。对为期２年的补钾补钙随机双盲安慰剂对照试验的２６１名儿童进行了盐敏感性测定。结果显示：盐敏感性儿童，补钾补钙组２年期血压增长值较安慰剂组低４．３／４．８ｍｍＨｇ（Ｐ＜０．０５），前者血压增长幅度较后者低３．６／７．０个百分点（Ｐ＜０．０５）；而盐不敏感儿童，补充组与安慰剂组间血压变化无显著性差异。盐敏感性儿童经补钾补钙后，夜８小时尿钠排泄量明显增加（Ｐ＜０．０１），且后者与其血压增长幅度呈负相关（ｒ＝－０．３９，Ｐ＜０．０１）。提示，适量增加钾和钙的摄入，通过与钠离子的相互复合作用，促进尿钠排泄，可降低盐敏感儿童血压的增长幅度。     

3岁～6岁儿童脉压分布特征及其影响因素

目的 探讨脉压（pp）在3岁～6岁儿童的分布特征。方法 对云南2002年16个地区12个民族城乡3岁～6岁儿童共15877人按国际统一标准测量血压，同时对人群中不同性别、不同年龄组的pp、血压水平以及影响进行分析。结果 随着血压的增高，pp的分布频率也在增高，血压正常儿童PP30mmHg～40mmHg频度最高，农村儿童平均收缩压（SBP）和舒张压（DBP）均高于城市儿童，SBPU值为6、94，P〈0．01，DBPU值为5．40，P〈0．05，农村儿童高血压患病率高于城市儿童，但只有收缩压有显著意义。结论 脉压大于40mmHg时是儿童高血压易患的一个信号，农村儿童优质蛋白质较低是影响血压水平的可能因素。     

低钠富钾替代盐对农村社区人群血压影响的现场观察

该文评价市售低钠富钾替代盐对农村社区居民血压的影响效果。方法:采用流行病学类实验设计,在山东省莱芜市2个农村社区,经过血压筛查,将411名30～60岁的研究对象分为高血压组和非高血压组,两     

有或无高血压家属性倾向的青年男性改变饮食中钠、钾含量对血压及激素的影响

早先的研究发现,将饮食中的钠、钾比例减少三个月,可使轻度高血压患者的血压显著降低,正常血压的对照者则无改变,本文报道改变饮食中钠、钾含量对有高血压家属性倾向的年轻人的影响。方法:23名20～26岁的男性医学生,分为二组。第一组12名的双亲中一人或二人血压超过150/90毫米汞柱,正在作高血压治疗或死于高血压并发     

长沙市9～14岁儿童血压调查报告

为探讨儿童血压的影响因素，对长沙市496名9～14岁儿童进行血压调查，结果表明，年龄、性别、身高、体重对血压均有影响，尤以身高、体重为著。在此基础上提出9～14岁儿童高血压诊断的参考标准。     

儿童血压与体重、红细胞钠、钾及遗传关系的流行病学调查

笔者研究了3063名0～15岁儿童血压与身高、体重、红细胞钠、钾浓度及遗传家系史的关系。经统计学处理证明:儿童血压随年龄、身高、体重增长而升高;高血压者与血压正常者红细胞内钠、钾、血浆钠浓度随年龄增长而增高,两者有明显差异。     

3～6岁儿童肥胖度对血压影响的调查分析

目的 :调查分析 3～ 6岁的学龄前儿童肥胖度与血压测量值的相关关系、肥胖度分层对血压的影响。　　方法 :整群抽取广东省韶关市区四所幼儿园的 3～ 6岁儿童作为调查对象。测量身高、体重、血压 ,分析肥胖度与血压测量值之间的相关关系。将儿童按每周岁一个年龄组分为 4组 ,分析肥胖、超重、消瘦、正常各层 4组间血压测量值的差异以及各年龄组肥胖、超重、消瘦、正常各层间血压测量值的差异。　　结果 :分析显示肥胖度与收缩压及舒张压之间均呈明显的正相关关系。 4组肥胖、超重、消瘦、正常各层间收缩压和舒张压测量值均存在非常显著的差异 (P <0 0 0 0 1)。　　结论 :学龄前儿童单纯肥胖已经对血压产生明显的影响。儿童肥胖的预防应早在学龄前期进行相关教育和行为干预。     

偶测正常血压老年糖尿病患者24小时动态血压分析

目的　探讨糖尿病患者在偶测血压增高之前动态血压是否变化。方法　从疗养人群中随机选择偶测血压正常的老年糖尿病患者 3 0例为 DM组、健康老年人 3 7例为对照组 ,比较两组动态血压的测试结果。结果　 (1 )糖尿病组 2 4小时平均血压、白天、夜间平均血压及 2 4小时波动曲线均显示血压高于对照组 ,其中 DM组 2 4小时 SBP、最小 SBP经统计学处理 ,P<0 .0 5。 (2 ) 2 4小时平均 SBP、日间、夜间平均 SBP超过正常参考标准的百分比 ,两组间比较有显著差异。 (3 ) DM组 SBP2 4小时压力负荷为 3 5 .4% ,对照组 SBP2 4小时压力负荷为 2 4.1 % ,但组间比较无显著差异。结论　偶测血压正常的糖尿病患者在血压增高之前 ,动态血压显示 2 4小时平均血压 ,已经高于对照组。     

儿童血压和嗜盐度相关性研究

<正> 流行病学研究提示,饮食中钠摄入量是影响血压水平的重要因素,应从多方面开展研究。作者采用测试嗜盐度的方法于1981和1985年对204名儿童的血压和嗜盐度进行了相关性研究。结果表明,血压正常的男性儿童其血压和嗜盐度呈正相关,女性儿童未见相关。材料和方法一、观察对象:1981年8～10月,在房山区农村,对同村居住的11～14岁共1141名男女儿童,测量了安静状态下右臂肱动脉血压。血压计气囊放气速度为2～3mmHg/秒。收缩压     

Sodium and Hypertension: Effect of Dietary Calcium Supplementation on Blood Pressure

Normotensive female Wistar Kyoto rats were studied to examine the effects of replacing drinking water with highly palatable saline solution at a concentration (0.5%) close to the maximum preferred concentration in these animals. A further group of animals was offered a calcium-supplemented diet in addition to substitution of drinking water with saline. Fluid consumption in animals drinking tap water was constant at between 35–40 ml/day throughout the six-month study period. In contrast, animals drinking 0.5% saline consumed 75–85 ml/day throughout the study period, irrespective of the calcium content of the diet. Voluntary consumption of these quantities of saline was associated with the development of a moderate hypertension, measured by tail cuff plethysmography, after two months of study. However, in animals consuming calcium-supplemented diets the hypertensive response disappeared after 3 months of study. Blood pressures were validated at the conclusion of the study by direct arterial cannulation and confirmed the presence of hypertension in saline drinking animals only when diets lacked calcium supplementation. No changes in blood ionized sodium concentration were associated with saline consumption; however, blood ionized calcium was significantly reduced in animals drinking saline, but not when calcium-supplemented diet was available. These studies suggest an interaction between sodium and calcium in the genesis of sodium-dependent hypertension.     

Dietary Calcium Intake and Blood Pressure in Normotensive Subjects

ABSTRACT. Epidemiological and prospective studies in man and animals have indicated an inverse relationship between calcium intake and cardiovascular mortality and blood pressure (BP). We have therefore studied the effect of dietary calcium on blood pressure in two groups of women. In a cross-sectional study 103 early postmenopausal women were stratified into three groups according to daily calcium intake calculated from a questionnaire. Both diastolic and systolic blood pressures were identical in the three groups. We thereafter conducted a prospective placebo-controlled trial on the effect of calcium supplementation. Twenty-eight healthy women were randomized to placebo treatment (n=14) or calcium supplementation 2000 mg daily (n=14) for one year. In both groups BP remained at initial levels throughout the study and was identical in the two groups at measurements every three months. We thus conclude that calcium supplementation has no effect on BP in normotensive subjects on a high calcium diet.     

The effect of sodium and potassium loading on urinary kallikrein-like activity in young patients with borderline hypertension

We studied the effects of a potassium supplement on urinary kallikrein excretion in a setting of high sodium intake after sodium deprivation with diuretics in young patients with borderline hypertension. Eleven patients, who took the potassium supplementation during the high sodium diet period, showed lower increments in mean blood pressure with salt loading than 12 patients without the potassium supplementation. In the non-potassium-supplemented patients, urinary kallikrein was increased significantly when plasma renin activity (PRA), plasma aldosterone concentration (PAC), and urinary aldosterone were increased during the diuretic treatment. It was decreased significantly when the other hormones were decreased during the sodium load. During the high sodium diet period, PRA, PAC and urinary aldosterone were greater in the potassium-supplemented patients than in the non-potassium-supplemented ones, but urinary kallikrein excretion was not higher when potassium was supplemented. Thus, the present results did not support the theory that the kallikrein-kinin system may be involved in the natriuretic and antihypertensive effects of potassium. In addition, these finding suggest that some kallikrein-modulating factor(s) may counteract the increased urinary kallikrein excretion with the augmented renin-angiotensin-aldosterone system during salt loading with potassium supplementation.     

Modification of intracellular calcium and plasma renin by dietary calcium in men

A double blind, placebo-controlled, parallel study was conducted on the effect of a high daily oral calcium supplementation of 1 g elemental calcium, given twice daily for 16 weeks in normal male subjects, on plasma renin, aldosterone, kallikrein, cGMP, cAMP, and calciotropic hormones, intracellular calcium concentrations, and plasma total and ionized calcium. After a 1-month run-in period on a limited use of dairy products, the subjects (n = 32) were allocated to a placebo or a calcium group. Placebo or 1 g elemental calcium was administered twice daily in the morning and evening for 16 weeks. All subjects were investigated at baseline and after 1, 2, 4, 8, and 16 weeks of placebo or calcium administration.

A decreased intraerythrocyte and intraplatelet Ca²⁺ concentration was observed in the calcium-treated subjects. Compared with the placebo group, an increase in the plasma renin activity (PRA) in the calcium group was observed after 4, 8, and 16 weeks of oral calcium administration. However, plasma aldosterone and urinary excretion of aldosterone, kallikrein, cGMP, and cAMP were not changed during calcium administration. Oral calcium supplementation in these men was also accompanied by a reduction in the plasma concentration of intact parathyroid hormone and 1,25-dihydroxyvitamin D₃, and an increase in 24-h urinary calcium excretion, but no change in the plasma total Ca²⁺ concentration, serum ionized Ca²⁺ level, and plasma phosphate or 25-hydroxyvitamin D₃.Our data show that the increase in PRA observed in men during oral calcium supplementation is accompanied by a reduction in the intracellular free and total Ca²⁺ concentration in platelets and erythrocytes and by a decrease in the plasma concentration of intact parathormone and 1,25-dihydroxyvitamin D₃.     

Effect of dietary sodium in hypertension not treated with drugs]

The usefulness of salt restriction in essential hypertension is still now disputed. This study was designed to test the influence of a diet with and without salt restriction in 19 untreated essential hypertensives (12 with and 7 without family history of hypertension) and free of cardiovascular and renal complications. Each patient was examined after a placebo period, after 1 month of salt restriction, and after 1 month of salt supplementation. Weight, blood pressure, 24 hours urinary sodium excretion and red blood cell ionic fluxes were measured. In patients with hypertensive heredity, the blood pressure did not change. The intracellular sodium concentration, the cotransport and the countertransport remained stable. The ouabain sensitive sodium pump slightly increased during salt restriction and remained stable after salt supplementation. In patients without such hypertensive heredity (who were older and heavier), sodium restriction period was characterized by significant decrease in blood pressure, weight, intracellular sodium concentration and increase in sodium pump activity. When salt was increased, all the parameters remained stable. A more balanced diet with sodium restriction decreases the blood pressure in relation to age, weight and the blood pressure level. Hypertensive heredity does not seem to be a parameter of salt sensitivity. The blood pressure decrease is also related to the quantitative importance of sodium restriction. The ouabain sensitive pump activity changes during diet especially in relation to weight loss and decreasing salt intake.     

Effect of potassium supplementation on blood pressure in Chinese: a randomized, placebo-controlled trial.

OBJECTIVE: To examine the effect of potassium supplementation on blood pressure (BP) in a Chinese population who consume a habitual high sodium and low potassium diet. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: Community sample from Beijing, China. PARTICIPANTS: A total of 150 men and women aged 35-64 years with an initial systolic BP 130-159 mmHg and/or diastolic BP 80-94 mmHg. INTERVENTIONS: Participants were randomly assigned to take 60 mmol potassium chloride supplement or placebo for 12 weeks. MAIN OUTCOME MEASURE(S): BP measurements were obtained at baseline, and at 6 weeks and 12 weeks during the trial, using random-zero sphygmomanometers. RESULTS: The average baseline urinary excretion of sodium and potassium was 182 mmol/24 h and 36 mmol/24 h. Baseline BP and other measured variables were similar between the potassium supplementation and placebo groups. In the active compared to the placebo treatment group, the urinary excretion of potassium was significantly increased by 20.6 mmol/24 h (P< 0.001) during 12 weeks of intervention. Compared to placebo, active treatment was associated with a significant reduction in systolic BP (-5.00 mmHg, 95% CI: -2.13 to -7.88 mmHg, P < 0.001) but not diastolic BP (-0.63 mmHg, 95% CI: -2.49 to1.23 mmHg, P = 0.51) during 12-week intervention. CONCLUSION: These data indicate that moderate potassium supplementation resulted in a substantial reduction in systolic BP. Our findings suggest that increased potassium intake may play an important role in the prevention and treatment of hypertension in China.     

The effects of aprotinin, a kallikrein inhibitor, on renin release and urinary sodium excretion in mild essential hypertensives

The effects of aprotinin on renin release and renal function were evaluated in 24 male essential hypertensive patients, on unrestricted (n = 17) and on chronic low as well as on high sodium intake. Aprotinin (1 X 10(6) kallikrein inhibitor units) or saline (200 ml) were infused in all patients for 6 h. Blood samples were taken for plasma renin activity (PRA) and 6-h urine collections were obtained for active and inactive kallikrein, sodium and potassium excretion measurement. In patients on unrestricted sodium diet, aprotinin had no effect on blood pressure (BP), glomerular filtration rate, renal plasma flow, urinary sodium and potassium excretion. However, an inverse relationship was found between pretreatment urinary sodium excretion and the per cent reduction of the latter after aprotinin. A significant reduction in urinary sodium excretion was induced by aprotinin in patients on high sodium intake, whereas no change was observed in the same patients when on a low sodium diet. Aprotinin reduced the urinary excretion of active kallikrein by 81% and the active to total kallikrein ratio from 24 to 6%. Infusion of aprotinin induced a significant decline in active renin but did not modify inactive renin levels in patients on unrestricted sodium diet as well as in patients on low or high sodium intake. Our data suggest that the inhibition of kallikrein and/or other serine proteases by aprotinin can interfere with renal release of active renin and also support the hypothesis that the renal kallikrein system exerts a regulatory control on sodium excretion in salt replete hypertensives.     

The role of melatonin in the pathogenesis of hypertension in rats with metabolic syndrome

BACKGROUND: Melatonin, the primary hormone of the pineal gland, is a known modulator of various physiological processes. The aim of this study was to evaluate the role of melatonin in the pathogenesis of hypertension in rats with metabolic syndrome and to assess whether melatonin supplementation prevents the development of hypertension in this model. METHODS: Twenty male Sprague-Dawley (SD) rats were fed either a high fructose diet (n = 10) or a regular diet (control; n = 10) for 5 weeks. Urinary excretion of 6-hydroxymelatoninsulfate (a metabolite of melatonin) was measured at the beginning and the end of the study. An additional 20 SD rats were fed with the same diets but with a supplementation of melatonin (30 mg/kg/day) in their drinking water. Blood pressure (BP) was measured every week. RESULTS: BP increased significantly in rats fed with a high fructose diet and remained unchanged in the control group. The BP rise was associated with a significant decrease in melatonin secretion during sleep. Melatonin supplementation prevented the BP rise in fructose fed rats. BP increased by 14.6 +/- 1.0 mm Hg in the fructose fed rats, whereas it increased by only 3 +/- 2.6 mm Hg in rats fed with fructose and melatonin (P < 0.001 between groups). CONCLUSIONS: Melatonin secretion decreased in fructose fed rats that developed hypertension. Administration of melatonin blunted this BP rise. These data suggested that melatonin plays a role in the pathogenesis of hypertension in rats with metabolic syndrome.     

Effect of oral sodium bicarbonate supplementation on interdialytic weight gain, plasma sodium concentrations and predialysis blood pressure in hemodialysis patients

BACKGROUND: Correction of metabolic acidosis in dialysis patients should be considered of paramount importance. However, consuming sodium bicarbonate tablets during the interdialytic interval to reach predialysis bicarbonate levels of 23--24 mmol/l is not widespread due to the fear of greater interdialytic weight gain and fluid overload. For this reason we investigated in a cross-sectional and in an interventional study the effect of oral sodium bicarbonate supplementation on body weight gain, plasma sodium concentrations and predialysis blood pressure in a group of stable uremic patients on regular hemodialysis (HD) treatment. Study DESIGN: 110 patients (67 men, 43 women), mean age 67+/-15 (range 22--89) years, on regular chronic HD treatment for 6--372 (median 48) months were studied. 70 patients were on regular oral bicarbonate supplementation for at least 4 weeks (group A), 40 patients were not on oral bicarbonate supplementation (group B). The following parameters were recorded: dry body weight (DBW), interdialytic weight gain (IWG), body mass index (BMI), plasma sodium (Na), serum pH, serum bicarbonate (sBic), K(t)/V, normalized protein catabolic rate (PCRn), predialysis systolic (SBP) and diastolic (DBP) blood pressure, and bicarbonate therapy (g/day). 18 patients not on oral bicarbonate supplementation with sBic levels相似文献   

Gestational calcium supplementation and blood pressure in the offspring

BACKGROUND: The current study examined the relationship between calcium supplementation during pregnancy and blood pressure (BP) in the mother and offspring at 3 months and at 2 years postpartum. METHODS: Nulliparous pregnant women were assigned to either receive 2 g of calcium or placebo daily beginning between weeks 13 to 21 of gestation and continuing until delivery. Blood pressure was measured in children and their mothers at 3 months (n = 260) and (n = 57) at 2 years postpartum. Systolic BP was measured in the infants using a sphygmomanometer with ultrasonic amplification. For the toddlers, three supine BP measurements were taken from the right arm using a Critikon automated sphygmomanometer just after measurement of left ventricular wall thickness. RESULTS: Systolic BP in the calcium-supplemented infants was 2.2 mm Hg lower than in the placebo group (P >.05). At 2 years of age, systolic BP was 4.8 mm Hg lower in the calcium supplemented group (P <.05), whereas diastolic BP was 3 mm Hg lower (P >.05). There was no difference in left ventricular mass index between groups, although there was a significant correlation between systolic BP and wall thickness (P <.05). Maternal BP was positively correlated with circulating 1,25(OH)(2)D3 (P <.001) but did not differ between calcium groups at 3 months postpartum. CONCLUSIONS: The data on BP in the children are in agreement with previous studies and argue strongly for additional research into the effects of prenatal calcium supplementation on BP regulation in the offspring.