钠钾对血压盐敏感者短时血压变异性的影响

目的观察血压盐敏感者在钠、钾饮食干预后短时血压变异性(BPV)的变化,探讨BPV与盐敏感的关系。方法 2004-04-10对陕西眉县农村正常血压成人93名进行低盐(氯化钠51.3mmol/d)饮食7d,高盐(氯化钠307.7mmol/d)饮食7d的慢性盐负荷试验,之后进行高盐补钾(307.7mmol/d氯化钠基础上口服60mmol/d氯化钾缓释胶囊)干预7d;每个阶段最后一天测3次血压,以血压标准差、变异系数为短时BPV指标。根据高盐饮食后平均动脉压升高幅度是否≥10%,分为血压盐敏感组(n=30)及盐不敏感组(n=63)。结果盐敏感性检出率为32.3%。基线期时,与盐不敏感组比较,盐敏感组收缩压标准差[(4.4±1.1)比(2.5±0.5)mmHg,P<0.01];舒张压标准差[(3.7±1.7)比(2.8±0.9)mmHg,P<0.01];收缩压变异系数[(3.78±1.01)比(2.35±0.55),均P<0.01];舒张压变异系数[(5.06±2.50)比(3.99±1.46),P<0.05]均较高。盐敏感组低盐期及高盐补钾期收缩压、舒张压标准差及变异系数均降低,与盐不敏感组比较,差异无统计学意义;予高盐饮食后,盐敏感组收缩压标准差较低盐期升高,与盐不敏感组比较,差异有统计学意义[(3.7±1.9)比(3.0±1.1)mmHg,P<0.05]。结论高盐摄入、盐敏感是短时BPV增大的重要原因,限盐及补钾具有降低短时BPV的保护作用。     

左旋精氨酸甲酯及左旋精氨酸对应激状态下胃黏膜耐受性细胞保护作用的影响

目的：探讨内源性一氧化氮（NO）在应激状态下胃黏膜耐受性细胞保护中的作用及其可能的机制。方法：以重复浸水束缚应激（WRS）制作动物模型,以左旋精氨酸甲酯（L－NAME）或左旋精氨酸（L－Arg）抑制或促进内源性NO的合成,动态检测胃黏膜血流量（GMBF）、溃疡指数（UI）、黏膜一化氮含量的变化。结果：重复应激后,实验对照组大鼠UI明显下降,同时GMBF上升,黏膜内NO含量增高;L－NAME使WWRS引起的胃黏膜损伤加重,消除了GMBF的递增趋势,黏膜NO含量下降;而L－Arg可减轻WRS造成的黏膜损伤,GMBF、黏膜NO含量增相应增加;GMBF、UI、黏膜NO含量变化之间有相关关系。结论：内源性NO通过调节GMBF而介导耐受性细胞保护作用,L－NAME抑制其合成,延缓这一作用,L－Arg增加其合成,促进该作用。     

青少年盐敏感者盐敏感性的远期可重复性及血压的增龄性改变

目的　观察青少年盐敏感性的可重复性 ,对比观察盐敏感与盐不敏感性青少年血压的增龄性改变。方法　 55名进行过急性盐水负荷和呋塞米缩容试验确定盐敏感性的青少年 ,于 5年后再次行静脉盐水负荷、呋塞米缩容试验 ,确定其盐敏感性的可重复性 ;比较 5年前、后均判定为盐敏感者的血压变化。结果　 (1 )静脉盐水负荷、缩容试验判定盐敏感性 5年后测定的可重复性为 92 7%。(2 )盐敏感组青少年 5年血压的增长值和增长幅度均高于盐不敏感组 ,分别为 9 9 4 7mmHg (1mmHg=0 1 33kPa)和 9 7 6 4个百分点 ,特别以收缩压最为显著 (P <0 0 1 )。结论　静脉盐水负荷试验确定盐敏感性具有良好的远期可重复性 ;青少年盐敏感者血压随年龄的增长幅度远高于盐不敏感者 ,特别是收缩压     

盐敏感者盐负荷期间交感神经活性研究

为探讨盐敏感性个体交感神经活性与盐负荷的关系，对２３例２３～４０岁的血压正常者采用慢性盐负荷的方法确定盐敏感者（ＳＳ），观察盐负荷期间以及冷加压试验中血浆去甲肾上腺素（ＰＮＥ）和血浆肾上腺素（ＰＥ）水平、心率变异性、动态血压、２４小时尿Ｎａ＋排泄量和红细胞Ｎａ＋含量等变化。发现与盐不敏感者（ＮＳＳ）相比，ＳＳ者于盐负荷及应激状态下伴随血压的升高，ＰＮＥ和ＰＥ均增高，尤以ＰＮＥ为著；心率变异性频域分析中夜间低频（ＬＦ）和ＬＦ与高频（ＨＦ）成份比值（ＬＦ／ＨＦ）增加；动态血压中的夜间血压偏高，昼夜血压差值缩小。盐负荷期间２４小时尿Ｎａ＋排泄量降低，红细胞Ｎａ＋含量显著升高，且前者与ＰＮＥ呈负相关（ｒ＝－０．５４，Ｐ＜０．０５）。上述结果表明，本研究年龄段的血压正常盐敏感者存在高盐介导的交感神经活性增高表现。     

血压盐敏感者一氧化氮系统与非对称性二甲基精氨酸和补钾的作用

目的通过观察慢性盐负荷及补钾后血浆非对称性二甲基精氨酸(ADMA)和血、尿一氧化氮(NO)水平的变化及其与血压的关系,探讨血压正常盐敏感者(SS)的血管内皮功能损伤及补钾的保护作用。方法选60例年龄在20～60岁的血压正常者参与为期3周的慢性盐负荷及补钾试验,包括基线调查3d,低盐(LS)饮食,高盐(HS)饮食,和高盐补钾(HS K)饮食各7d的研究。每个阶段均测量血压,并收集血、尿标本。血、尿NO用Griess法测量,血浆ADMA用高效液相色谱法测量。结果受试者60例中共检出SS13例,检出率为21.6%。盐负荷后,SS血浆ADMA的浓度明显升高[(0.89±0.09vs0.51±0.07)μmol/L,P<0.05],而血浆NO的水平则较LS饮食期显著降低[(41.8±7.6vs63.5±7.6)μmol/L,P<0.01]。在HS摄入的基础上大剂量口服补钾可以逆转单纯HS负荷对SS血浆ADMA浓度和血、尿NO水平的作用[(ADMA:0.52±0.09vs0.89±0.09)μmol/L;NO:(58.1±7.4vs41.8±7.6)μmol/L],血浆ADMA浓度和平均动脉压之间存在正相关关系。结论血压正常SS于HS负荷后伴随血压升高,血浆ADMA显著升高、NO降低,同时补充钾盐可以逆转前述作用,提示补钾可能通过抑制ADMA的升高降低血压。     

血压盐敏感者一氧化氮系统与非对称性二甲基精氨酸和补钾的作用

目的 通过观察慢性盐负荷及补钾后血浆非对称性二甲基精氨酸(ADMA)和血、尿一氧化氮(NO)水平的变化及其与血压的关系,探讨血压正常盐敏感者(SS)的血管内皮功能损伤及补钾的保护作用.方法选60例年龄在20～60岁的血压正常者参与为期3周的慢性盐负荷及补钾试验,包括基线调查3 d,低盐(LS)饮食,高盐(HS)饮食,和高盐补钾(HS K)饮食各7 d的研究.每个阶段均测量血压,并收集血、尿标本.血、尿NO用Griess法测量,血浆ADMA用高效液相色谱法测量.结果 受试者60例中共检出SS 13例,检出率为21.6%.盐负荷后,SS血浆ADMA的浓度明显升高[(0.89±0.09 vs 0.51±0.07)μmol/L,P＜0.05],而血浆NO的水平则较LS饮食期显著降低[(41.8±7.6 vs 63.5±7.6)μmol/L,P＜0.01].在HS摄入的基础上大剂量口服补钾可以逆转单纯HS负荷对SS血浆ADMA浓度和血、尿NO水平的作用[(ADMA:0.52±0.09 vs 0.89±0.09)μmol/L;NO:(58.1±7.4 vs 41.8±7.6)μmol/L],血浆ADMA浓度和平均动脉压之间存在正相关关系.结论 血压正常SS于HS负荷后伴随血压升高,血浆ADMA显著升高、NO降低,同时补充钾盐可以逆转前述作用,提示补钾可能通过抑制ADMA的升高降低血压.     

高血压盐敏感者肾脏锂清除率,肾血流动力学和尿微白蛋白排泄

目的探讨盐敏感者肾脏损害与肾脏钠代谢及肾血流动力学的关系，以期对盐敏感者肾损害的防治提供理论依据。方法６０例原发性高血压患者采用急性静脉盐水负荷法确定盐敏感性，并观察肾脏锂清除率，肾血流动力学改变及２４小时尿微白蛋白排泄量。结果与盐不敏感性高血压患者相比，盐敏感者肾脏锂清除率和锂排泄分数低，近端肾小管钠的重吸收率高于盐不敏感者；盐敏感者双肾血流量减低、滤过分数及肾血管阻力均高于盐不敏感者（Ｐ＜０．０１），２４小时尿微白蛋白排泄量高于盐不敏感者。结论盐敏感者存在盐负荷后肾血流动力学适应性调节异常及近端肾小管钠转运障碍，其肾功能损害可能较盐不敏感者出现早。     

慢性盐负荷对血压盐敏感者血浆内皮生长因子C的影响

目的 本研究通过对正常血压受试者进行饮食干预试验,观察高盐对盐敏感者血浆内皮生长因子C(VEGF-C)的影响,探索淋巴系统在盐敏感性形成过程中的作用。方法对27例血压正常受试者进行7 d低盐、7 d高盐饮食干预,采用国际慢性盐负荷试验鉴别盐敏感者,筛选出盐敏感者9例,盐不敏感者18例,采用ELISA方法测定血浆VEGF-C的含量。结果两组受试者低盐期血浆VEGF-C水平比较无统计学差异〔(1921±238) mg/L vs.(1804±206) mg/L,P=0.59〕,而高盐干预后两组血浆VEGF-C水平均较低盐期明显增加〔盐敏感组(3642±406) mg/L,盐不敏感组(2249.8±214.6) μg/ml〕,并且高盐干预后盐敏感组VEGF-C水平较盐不敏感组显著升高（P<0.01）;相关分析表明,血浆VEGF-C水平与血压之间未发现具有统计学意义的相关性（r=0.412,P=0.29）。结论高盐饮食后盐敏感者体内VEGF-C显著升高,而VEGF-C可能成为盐敏感性识别的重要生化标记物之一。     

正常血压颈动脉狭窄患者血压水平与颈动脉血流的关系

目的 通过彩超检查研究正常血压颈动脉狭窄患者血压水平与颈动脉血流参数的关系.方法 对80例至少一侧颈动脉狭窄≥30%的正常血压患者进行血压测量和彩色多普勒超声检查,检查指标包括收缩压、舒张压、双侧颈动脉血流动力学参数.结果 狭窄程度增大,狭窄侧颈内动脉血流速度增大.健侧(或狭窄较轻侧)椎动脉血流速度分别在90～120 mmHg组及60～79 mmHg组流速较大,随血压增高而降低;健侧(或狭窄较轻侧)颈内动脉和椎动脉血流阻力指数分别随着收缩压及舒张压水平的增高而增大,且椎动脉搏动指数也随舒张压的增高而增大.血压增高到收缩压>120 mmHg、舒张压≥80 mmHg时流速明显降低,血流阻力增大.结论 狭窄程度相同时,正常血压患者控制血压水平有利于增加脑血供;收缩压90～120 mmHg、舒张压60～79 mmHg可维持正常血压颈动狭窄患者较好的脑血供.     

Cosegregation Analysis of Salt Appetite and Blood Pressure in Genetically Hypertensive and Normotensive Rats

Enhanced sodium appetite is a robust behavioral characteristic of spontaneously hypertensive rats (SHR) which neither causes nor depends upon elevated blood pressure. However, the possibility remains that salt appetite and blood pressure are related by some unidentified common factor. The present study investigated the possible genetic co-determination of blood pressure and salt appetite in this animal model of hypertension.

Blood pressure of SHR, Wistar/Kyoto (WKY), and their F1 and F2 populations was measured prior to salt appetite testing by the tail cuff method. Sodium intake in these groups was measured daily for 5 days as the ad lib consumption of a 1.5% NaCl solution by subjects maintained on sodium deficient chow and demineralized water. Dynamic and stable components of salt appetite were identified in the parent strains and analyzed in the hybrid offspring.

The expected differences in blood pressure between SHR and WKY were observed, and the average blood pressure of the F1 and F2 groups fell roughly midway between SHR and WKY values. The SHR consumed substantially greater quantities of saline than WKY, but the F1 population consumed saline at a rate that was not different from WKY, rather than intermediate between SHR and WKY. There was no relationship in the F2 population between blood pressure and any measure of salt appetite. Thus, the high salt appetite and high blood pressure traits of SHR do not appear to share a common genetic basis. These results, considered with previously published work, suggest that approach and avoidance aspects of salt appetite may be separately inherited and also strongly suggest that neither is linked to hypertension.     

动态血压监测在评价慢性肾脏病合并高血压患者血压达标中的价值

目的 比较动态血压及诊室血压评价慢性肾脏病（CKD）合并高血压患者血压达标率的差异。方法 选取2012年5月～2013年2月在中南大学湘雅三医院就诊的225例慢性肾脏病合并高血压患者。收集并分析研究对象的人口学、实验室检查及血压资料。结果 （1） 诊室血压监测和动态血压监测均随着肾功能恶化,血压达标率下降。其中诊室收缩压达标率CKD5期较CKD1～2期下降有统计学意义（18.3%比36.6%,P<0.05）,动态血压监测平均血压、日间收缩压、夜间血压达标率CKD5期较CKD1～2期下降均有统计学意义（P<0.05）。（2） CKD1～2期患者动态血压高血压检出率高于诊室血压高血压检出率（79.6%比61.3%,P0.038）,而CKD5期患者动态血压高血压检出率低于诊室血压高血压检出率（83.5%比93.0%,P0.029）。结论 （1） 随着肾功能恶化,CKD合并高血压患者血压达标率逐渐降低;（2）仅使用诊室血压评价CKD患者血压是否达标及昼夜血压达标情况存在不当,推荐CKD合并高血压患者使用动态血压监测。     

Blood Pressure and Metabolic Effects of ACTH in Normotensive and Hypertensive Man

ACTH administration (0.5 mg Synacthen Depot I/M 12 hourly for 5 days) significantly increased systolic blood pressure in normotensive subjects (n=6) and mild essential hypertensives (n=6) but not in 2 Addisonian women, indicating that the pressure rise was adrenally dependent. ACTH administration was associated with urinary sodium retention, hypokalaemia, elevation of fasting blood glucose, lymphopaenia and eosinopaenia. Body weight was increased only in the normotensive subjects. Plasma renin concentration fell and renin substrate rose. Inactive renin fell in the hypertensive subjects only. Plasma cortisol, 11-deoxycortisol, corticosterone, deoxycorticosterone, 17α-hydroxyprogesterone and 17-hydroxy, 20-dihydroprogesterone were all increased by ACTH treatment. Plasma aldosterone rose initially in the normotensives but then fell. ACTH administration in man produces metabolic and hormonal changes similar to those produced by ACTH in sheep but the rise in bloodpressure is systolic only in man. The steroid(s) responsible for the blood pressure rise with ACTH in man have not been defined.     

盐与高血压研究进展

大量流行病学调查及实验研究表明,盐作为重要的环境因素与高血压的发生发展密切相关,其不仅影响了血压调节,而且还可能独立于血压对心、脑、肾等器官的损害产生作用。此外通过研究肾脏排钠与高血压的关系也已筛选出许多与高血压有关的易感基因。本文就以上几方面对盐与高血压的研究进展作一综述。     

Hypotensive Properties of the Protein Kinase Inhibitor,Staurosporine, in Normotensive and Spontaneously Hypertensive Rats

The protein kinase inhibitor, staurosporine, was examined for hemodynamic actions in conscious rats and for its effects on isolated vascular smooth muscle. In conscious normotensive rats, staurosporine, 0.1 to 1.0 mg/kg intravenous, produced a dose-related decrease in blood pressure. Doses of 0.1 and 0.5 mg/kg produced reflex tachycardia, while heart rate decreased following 1.0 mg/kg. Higher doses of staurosporine (5 and 10 mg/kg), although not significantly altering heart rate, caused a precipitous drop in blood pressure and all rats died within 48 hours of treatment. Spontaneously hypertensive rats were significantly more sensitive than normotensive rats to the blood pressure lowering effects of staurosporine. The depressor activity of staurosporine was also observed in cord-stimulated pithed rats indicating that hypotension is a peripherally-rather than centrally-mediated effect of staurosporine. In ring preparations of rat thoracic aorta, staurosporine (3 nM to 0.1 mM) produced a concentration-dependent inhibition of serotonin-induced contraction, consistent with its ability to lower blood pressure by an effect at a peripheral vascular site. These results provide the first documentation of the potent cardiovascular activity of staurosporine in the conscious rat and support the contention that protein kinases, in particular protein kinase C, may be important in the regulation of vascular tone.     

Differential Effects of Ethanol on Baroreceptor Heart Rate Responses of Conscious Spontaneously Hypertensive and Normotensive Rats

This study investigated the acute effects of ethanol (0.25, 0.5, or 1 g/kg, iv) on mean arterial pressure, heart rate, and gain of the baroreceptor reflex control of heart rate (BRS) in conscious spontaneously hypertensive rats (SHRs) and age-matched Wistar rats. BRS was substantially lower in the SHRs as compared with the Wistar rats when measured by phenylephrine (-0.95 ± 0.16 vs. -2.02 ± 0.22 beats/min/mm Hg) or nitroprusside (-1.90 ± 0.2 vs. -3.02 ± 0.32 beats/min/mm Hg). None of the doses of ethanol influenced BRS in the SHR. In contrast, ethanol attenuated BRS in Wistar rats, but this effect was dependent on the dose used and the type of response. The lower doses attenuated the reflex tachycardic response, but had no effect on the reflex bradycardic response. On the other hand, the 1 g/kg dose of ethanol attenuated the reflex bradycardic but not the tachycardic response. Ethanol produced a pressor effect (15-25 mm Hg; 5-min duration), which was neither dose- nor strain-dependent. However, only in the SHR mean arterial pressure remained elevated (10-15 mm Hg above control) for 20 min in response to the 0.5 g/kg dose of ethanol, and its recovery coincided with the occurrence of a slowly developing negative chronotropic response. Ethanol produced a dose-related negative chronotropic effect in both strains of rats that was of longer duration in the SHR, particularly with the 1 g/kg dose. It is possible that the bradycardic effect of ethanol influenced negatively its pressor effects. Data suggest that, in conscious rats, ethanol: (1) attenuates BRS in normotensive rats but not in the SHR; (2) causes a brief pressor effect that is not related to its dose, the level of arterial pressure, or its influence on the gain of the baroreceptor reflex; and (3) elicits dose-related bradycardic responses that are of longer duration in the SHR, particularly with the higher dose. This negative chronotropic effect of ethanol may limit its pressor effect in SHRs.     

Impact of Light Salt Substitution for Regular Salt on Blood Pressure of Hypertensive Patients

Background

Studies have shown sodium restriction to have a beneficial effect on blood pressure (BP) of hypertensive patients.

Objective

To evaluate the impact of light salt substitution for regular salt on BP of hypertensive patients.

Methods

Uncontrolled hypertensive patients of both sexes, 20 to 65 years-old, on stable doses of antihypertensive drugs were randomized into Intervention Group (IG - receiving light salt) and Control Group (CG - receiving regular salt). Systolic BP (SBP) and diastolic BP (DBP) were analyzed by using casual BP measurements and Home Blood Pressure Monitoring (HBPM), and sodium and potassium excretion was assessed on 24-hour urine samples. The patients received 3 g of salt for daily consumption for 4 weeks.

Results

The study evaluated 35 patients (65.7% women), 19 allocated to the IG and 16 to the CG. The mean age was 55.5 ± 7.4 years. Most participants had completed the Brazilian middle school (up to the 8th grade; n = 28; 80.0%), had a family income of up to US$ 600 (n = 17; 48.6%) and practiced regular physical activity (n = 19; 54.3%). Two patients (5.7%) were smokers and 40.0% consumed alcohol regularly (n = 14). The IG showed a significant reduction in both SBP and DBP on the casual measurements and HBPM (p < 0.05) and in sodium excretion (p = 0.016). The CG showed a significant reduction only in casual SBP (p = 0.032).

Conclusions

The light salt substitution for regular salt significantly reduced BP of hypertensive patients.     

L-精氨酸抗家兔动脉粥样硬化内皮损伤

将新西兰兔分成三组：正常组、高胆固醇组、高胆固醇加Ｌ－精氨酸组。分别喂养４周和８周。扫描电镜下观察到：高胆固醇组与高胆固醇加Ｌ－精氨酸组相比，内皮细胞排列不规则，细胞间隙银染较粗，内膜损伤和增生明显。说明补充Ｌ－精氨酸可减轻内膜损伤。     

Effects of Neuropeptide Y on Cardiac Performance and Renal Blood Flow in Conscious Normotensive and Renal Hypertensive Rabbits

The effects of neuropeptide Y (NPY, 10 ug/kg bolus iv) on cardiac output, renal blood flow and myocardial contractility were determined in intact renal hypertensive and normotensive rabbits instrumented with ultrasonic flow transducers or left ventricular catheters.

The basal plasma concentration of NPY-like immunoreactivity in arterial blood was greater in the hypertensive rabbits (4.2 ± 0.7 ug/1) than in normotensive animals (2.2 ± 0.4 ug/l, p < 0.05). There were similar moderate increases in arterial blood pressure and total peripheral resistance following NPY, but a small NPY-induced reduction in cardiac output in normotensive rabbits was not seen in hypertensive animals. Resting peak left ventricular dP/dt (an index of myocardial contractility) was higher in hypertensive rabbits (73972 ± 619 vs 5551 ± 2342 mmHg/sec, p < 0.05), but there was no significant difference between the maximum NPY-induced falls in peak dP/dt.

NPY produced significant peak reductions in renal blood flow in both hypertensive (from 2.5 ± 0.2 to 1.22 ± 0.2 kHz, p < 0.05) and in normotensive rabbit groups (from 2.2 ± 0.1 to 0.3 ± 0.1 kHz, p<0.05), but the fall in renal blood flow and the corresponding rise in renovascular resistance were smaller in the hypertensive animals (p < .0 5). The cause of this apparent decrease in renovascular reactivity in the renal hypertensive model was not determined.