The Effect of Baroreflex Function on Blood Pressure Variability

Objective: The aim of this study was to assess the relationship of blood pressure variability (BPV) and heart rate variability (HRV) to investigate the effect of baroreflex function on blood pressure variability. Methods: This study consisted of 111 subjects, including 32 normotensives and 79 hypertensives. All the subjects were given two concurrent tests: 24-hour Holter ECG and ambulatory blood pressure monitoring. According to standard deviation of normal-to-normal sinus RR intervals (SDNN) derived from the Holter ECG, the hypertensives were divided into two groups: an HRV normal group with SDNN > 100 ms and an HRV abnormal group with

Ketanserin improves cardiac performance after myocardial infarction in spontaneously hypertensive rats partially through restoration of baroreflex function

Aim Baroreflex dysfunction is associated with a higher rate of sudden death after myocardial infarction （MI）. Ketanserin enhances baroreflex function in rats. The present work was designed to examine whether ketan- serin improves the post-MI cardiac function and to explore the possible mechanism involved. Methods Spontane- ously hypertensive rats （SHR） were treated with ketanserin （0.3 mg · kg^-1 · d^-l）. Two weeks later, blood pres- sure and baroreflex function were measured, followed by a ligation of the left coronary artery. The expressions of ve- sicular acetylcholine transporter （VAChT） and α7 nicotinic acetylcholine receptor （α7-nAChR） in ischemic myo- cardium, angiogenesis, cardiac function, and left ventricular （LV） remodeling were evaluated subsequently. Re- sults Ketanserin significantly improved baroreflex sensitivity （0.62 ± 0. 21 vs. 0.34 ± 0. 12 ms/mmHg, P 〈 0.01 ） and vagal tonic activity （ heart rate changes in response to atropine, 54.8 ± 16.2 vs. 37.6 ± 13.4 b. p. m. , P 〈 0.01 ） without affecting the blood pressure or basic heart rate in SHR. Treatment of SHR with ketanserin promi- nently improved cardiac function and alleviated LV remodeling, as reflected by increases in the ejection fraction, fractional shortening, and LV systolic pressure as well as decreases in LV internal diameter and LV relative weight. The capillary density, vascular endothelial growth factor expression, and blood flow in the ischemic myocardium were significantly higher in the ketanserin-treated group. In addition, ketanserin markedly increased the expression of VAChT and α7-nAChR in ischemic myocardium. Conclusion Ketanserin improved post-MI cardiac function and angiogenesis in ischemic myocardium. The findings provide a mechanistic basis for restoring baroreflex function using ketanserin in the treatment of MI.

Baroreflex deficiency aggravates learning and memory disorders in rats

OBJECTIVE Microglia M1/M2 po⁃larization play pro-inflammatory and anti-inflam⁃matory roles,respectively,which is involved in memory decline.There is a close relationship between impaired baroreflex function and memory impairment.The present study was designed to investigate whether arterial baroreflex deficiency induced by sinoaortic denervation(SAD)affected inflammation through modulation of M1/M2 polar⁃ization leading to the aggravation of learning and memory disorders in rats.METHODS Adult male SD rats were divided into four groups:the sham control,the SAD,the sham+scopolamine,the SAD+scopolamine.In another experiment,there were also four groups:the sham control,the SAD,the SAD+scopolamine and the SAD+scopolamine+ketanserin.All rats were examined for various behaviors using Morris water maze test,new object recognition test,and light dark shuttle test and Y maze test 4 weeks after sham or SAD surgery.CD16,CD206,IL-10,IL-6,IL-1βand TNF-αfrom hippocampus using Western blotting,immunofluorescence and turbidimetry.RESULTS Compared with the sham+scopol⁃amine,the SAD+scopolamine rats showed the reduced crossing times in Morris water maze test,the longer residence time in dark box during light dark shuttle test,and the decreased alterna⁃tion ratio in Y maze test.The level of CD206,IL-10,T-AOC and GSH was decreased,whereas CD16,IL-6,TNF-α,MDA was increased in the hippocampus of SAD+scopolamine rats.Addi⁃tionally,all the above changes were improved in the SAD+scopolamine+ketanserin rats when compared with the SAD+scopolamine.CONCLU⁃SION Arterial baroreflex dysfunction aggravates learning and memory disorders in rats,which may be related to the polarization of microglia.

Baroreflex impairment exacerbates LPS-induced inflammation in rat cerebral cortex and hippocampus

OBJECTIVE Platelets play a major role in mediating inflammatory response.The present work was designed to investigate whether arterial baroreflex impairment induced by sinoaortic denervation(SAD)affect platelet activation,leading to the exacerbation of cerebral cortex and hippocampus inflammation in rats.METHODS Adult male SD rats were divided into four groups:the sham control,the sinoaortic denervation(SAD),the sham+LPS,the SAD+LPS.In another experiment,there were also four groups:the sham control,the SAD,the SAD+LPS and the SAD+LPS+asprin.Four weeks after sham or SAD surgery,all rats were examined for the level of CD41,CD45,IL-1βand PF-4 in the cerebral cortex and hippocampus using immunofluorescence and ELISA.Blood platelet and leukocyte count,platelet microaggre⁃gation,expression of CD154 and CD62P on platelet surface and platelet-leukocyte aggregate level was detected by flow cytometry.RESULTS Compared with sham+LPS group,the in SAD+LPS group rats exhibited the high level of CD41,CD45,IL-1βand PF-4 in the cerebral cortex and hippocampus.Leukocyte count,platelet microag⁃gregation,expression of CD154 and CD62P on platelet surface and platelet-leukocyte aggregate level was increased,while blood platelet count was decreased in the SAD+LPS.Moreover,all the above changes were improved in the SAD+LPS+asprin group when compared with the SAD+LPS group.CONCLUSION Arterial baroreflex dysfunction exacerbates inflammation in the rat cerebral cortex and hippocampus,which is likely mediated by platelet.

Spontaneous Baroreflex Sensitivity in Normotensive African-American Men

Purpose: African-American men (AAM) have a greater risk of hypertension (HTN) than Caucasian men (CM). To reduce this risk, determining the differences in mechanisms involved in HTN and understanding the relationship between these mechanisms and factors affecting blood pressure (BP) in AAM and CM is necessary. One such mechanism is spontaneous baroreflex sensitivity (sBRS) and two factors are cardiorespiratory fitness (CRF) and arterial stiffness (AS). The aims of this study were to determine, firstly, whether there are differences in sBRS between young, normotensive AAM and CM, and secondly, to determine if CRF and AS are significant predictors of sBRS in young, normotensive AAM and CM. Methods: Twenty-three normotensive AAM and 36 CM were recruited from Southern Connecticut State University. Measures included anthropometric, sBRS (alpha-index), and CRF (maximal oxygen consumption [VO2max]), as well as AS (carotid-femoral pulse wave velocity [Cf-PWV]). Independent t-tests were used to determine differences between groups and multiple regression analysis was used to determine how much of the variation in sBRS was explained by CRF and AS. Results: The sBRS was significantly lower in AAM (10.3 ± 3.8 ms/mmHg) vs. CM (13.3 ± 5.7 ms/ mmHg), P = 0.03. CRF and AS were not significant predictors of sBRS in AAM (P = 0.25) and CM (P = 0.30). There was no relationship between, sBRS, CRF and AS;CRF was significantly reduced in AAM vs. CM (45.1 ± 6.3 vs. 52.1 ± 7.5 mL·kg?1·min?1, P ≤ 0.001). Conclusions: Young normotensive AAM demonstrated significantly lower sBRS vs. CM, irrespective of having fair CRF and normal BP. CRF and AS are not significant predictors of sBRS in young, normotensive AAM and CM. The attenuation in sBRS in AAM did not result in AAM having higher BP versus CM. This finding underscores the need for more detailed examination of the role of sBRS in the etiology of HTN in AAM.

Deterioration in Hemodynamics Reaction, Baroreflex Sensitivity, Sympathetic Nerve Activity and Redox State of Thoracic Aorta in the Experimental Model of Nitrate Tolerance and Its Pharmacological Correction

Continuous treatment with organic nitrates causes nitrate tolerance and provides evidence for a relationship between mitochondrial complex 1 activity and mitochondrial aldehyde dehydrogenase-2 (ALDH-2) with disturbances of the hemodynamics reaction during nitroglycerin (NTG) tolerance (NTGT). The purpose of this study was the evaluation of efficacy of original oxidized form NAD-containing drug, NADCIN®, on hemodynamic reactions, baroreflex sensitivity (BRS) and reflex control of splanchnic sympathetic nerve activity (SSNA), level of redox-potential, activity of ALDH-2 and superoxide anion generation in aortic tissue in rat model of NTGT. Five groups (7 - 9 each) of male Wistar rats, including control, acute i.v. NTG (150 mcg/kg) administration, NTG tolerance NTGT treatment with NADCIN® 8 mg/kg and methylene blue (MB, 2.5 mg/kg) were used. NTGT in rats was accompanied with the greatly attenuation of hemodynamics reaction, BRS, the decreasing of the ability to reflex control of SSNA without pronounce overexpression of endothelin-1 in vessels (aorta). In NTGT rats i.v. NTG along induced less hypotensive reactions and alterations in heart period vs single NTG treated group, more expressively decreased BRS (-34%) and reflex control of SSNA (-18%). NADCIN® significantly inhibits tolerance-inducing properties of the prolonged nitroglycerin infusion (max decrease of blood pressure response to nitroglycerin injection, % of normal controls: NTGT 51.2%, NADCIN® 91.6%, MB 55.8%). NADCIN® in NTGT rats after NTG i.v. administration increased reduced BRS (+37.8%, p < 0,05), reflex control of SSNA (+29.4%, p < 0.05) and reversed the decreasing of NAD/NADH ratio, ALDH-2 activity and decreasing in superoxide generation in thoracic aortic tissue. Thus, course treatment with NADCIN® of NTGT rats restores hemodynamics changes, BRS and SSNA throughout the increasing of redox-potential NAD/NADH and cessates the NTGT developing.

The Changes of Baroreflex Sensitivity During Head-up Tilt Test and Its Clinical Significance in the Patients with Vasovagal Syncope

Objective To study thechanges of baroreflex sensitivity (BRS) during head - up tilt test (HUT) in patients with vasovagal syncope (VS), and to examine the relationship between baroreflex sensitivity and neurohormonal factors. Furthermore, to investigate the effects of the changes of BRS on VS. Methods Forty - two patients with unexplained syncope (Among the 42 patients, there were 22 patients with positive HUT and 20 patients with negative HUT respectively) and 20 healthy volunteers (with negative HUT) underwent passive head - up tilt testing, Ante-cubital vein blood samples were taken before and after HUT, or at syncope. The fasting plasma endothelin , serum nitric oxide (NO), serum NE were measured, the BRS was assessed on the basis of the linear regression slope the RR interval versus systolic arterial blood pressure during the increment in blood pressure after intravenous administration of phenylephrine. Results (1) During the syncope, the BRS significantly reduced in HUT(+) group than baseline. At the end of tilt, the level of plasma ET, serum NO in patients with positive HUT significantly increased compared with baseline or normal controls, and the plasma concentration of NE also had the trend of increase. (2) By multiple regression analysis, a significant negative correlation was found between baroreceptor sensitivity and the plasma ET, NO at the end of HUT in patients with positive HUT, but there was no relationship between BRS and NE. Conclusions During the syncope occure, the BRS in patients with VS decreased significantly compared with normal controls. The abnormal plasma ET, NO concen-tration might contribute to the mechanism of VS.

Baroreflex dysfunction in chronic kidney disease

Chronic kidney disease(CKD) patients have high cardiovascular mortality and morbidity. The presence of traditional and CKD related risk factors results in exaggerated vascular calcification in these patients. Vascular calcification is associated with reduced large arterial compliance and thus impaired baroreflex sensi-tivity(BRS) resulting in augmented blood pressure(BP) variability and hampered BP regulation. Baroreflex plays a vital role in short term regulation of BP. This review discusses the normal baroreflex physiology, methods to assess baroreflex function, its determinants along with the prognostic significance of assessing BRS in CKD patients, available literature on BRS in CKD patients and the probable patho-physiology of baroreflex dysfunction in CKD.

Exploration of cardiac rehabilitation nursing for elderly patients with myocardial infarction based on individualized cardiac rehabilitation

BACKGROUND Myocardial infarction is a high-risk condition prevalent among the elderly population,often leading to adverse clinical manifestations such as reduced cardiopulmonary function,anxiety,and depression post-surgery.Consequently,cardiac rehabilitation holds immense importance in mitigating these complications.AIM To evaluate the effect of individualized cardiac rehabilitation on blood pressure variability(BPV)and baroreflex sensitivity(BRS)in elderly patients with myocardial infarction.METHODS A cohort of 74 elderly patients diagnosed with myocardial infarction and admitted to our hospital between January 2021 and January 2022 were subjected to random selection.Subsequently,all patients were divided into two groups,namely the research group(n=37)and the control group(n=37),utilizing the number table method.The control group received conventional drug treatment and nursing guidance intervention,while the study group underwent individualized cardiac rehabilitation in addition to the interventions received by the control group.All patients were continuously intervened for 12 wk,and the BPV of these two groups in the 1st wk(T0),the 4th wk(T1)and the 12th wk(T2)were compared,BRS,changes in cardiopulmonary function measures,and adverse cardiovascular events.RESULTS Of 24 h diastolic BPV,24 h systolic BPV,carbon dioxide ventilation equivalent slope of the research group were lower than those of the control group at T1 and T2,BRS,peak heart rate and systolic blood pressure product,1 min heart rate recovery were higher than those of the control group,and the incidence of adverse events in the research group was lower than that of the control group,the difference was statistically significant(P<0.05).CONCLUSION In this study,we found that after individualized cardiac rehabilitation in elderly patients with myocardial infarction,BPV and BRS can be effectively improved,cardiac function is significantly enhanced,and a better prognosis is obtained.

传入压力反射衰竭合并低钠血症1例

传入压力反射衰竭(afferent baroreflex failure,ABF)是一种罕见的疾病,该病是指由压力反射传入支或髓质水平的中央连接受损引起的临床综合征。本文报道1例颈部放射治疗及颈淋巴结清扫术后ABF导致波动性高血压合并神经源性直立性低血压(neurogenic orthostatic hypotension,nOH)及低钠血症的患者,以期警示临床医生关注颈部放射治疗或颈部手术患者。

压力感受性反射在疼痛调控中的机制及临床应用

压力感受性反射是自主神经系统维持心血管稳态的重要机制,其与疼痛调控亦存在密切关系。压力反射敏感性(baroreflex sensitivity,BRS)是定量评估压力感受性反射功能的指标,BRS下降与疼痛敏感性上升存在相关性,在疼痛风险预测、治疗效果评估中应用前景广阔。迷走神经刺激能够激活压力感受性反射,近年来在急慢性疼痛患者中得到了广泛应用。本文就压力感受性反射在疼痛调控中的机制和临床应用进行概述,以期为探索调节压力感受性反射功能的疼痛治疗手段提供新思路。

Anti-Hypertensive Action of Fenofibrate via UCP2 Upregulation Mediated by PPAR Activation in Baroreflex Afferent Pathway

Fenofibrate, an agonist for peroxisome proliferator-activated receptor alpha(PPAR-a), lowers blood pressure, but whether this action is mediated via baroreflex afferents has not been elucidated. In this study, the distribution of PPAR-a and PPAR-c was assessed in the nodose ganglion(NG) and the nucleus of the solitary tract(NTS). Hypertension induced by drinking high fructose(HFD) was reduced, along with complete restoration of impaired baroreceptor sensitivity, by chronic treatment with fenofibrate. The molecular data also showed that both PPAR-a and PPAR-c were dramatically up-regulated in the NG and NTS of the HFD group. Expression of the downstream signaling molecule of PPAR-a, the mitochondrial uncoupling protein 2(UCP2), was up-regulated in the baroreflex afferent pathway under similar experimental conditions, along with amelioration of reduced superoxide dismutase activity and increased superoxide in HFD rats.These results suggest that chronic treatment with fenofibrate plays a crucial role in the neural control of blood pressure by improving baroreflex afferent function due at least partially to PPAR-mediated up-regulation of UCP2 expression and reduction of oxidative stress.

Contribution of Baroreflex Afferent Pathway to NPY-Mediated Regulation of Blood Pressure in Rats

Neuropeptide Y (NPY), a metabolism-related cardiovascular factor, plays a crucial role in blood pressure(BP) regulation via peripheral and central pathways. The expression of NPY receptors (Y1R/Y2R) specific to baroreflex afferents impacts on the sexually dimorphic neural control of circulation. This study was designed to investigate the expression profiles of NPY receptors in the nodose ganglion (NG) and nucleus tractus solitary (NTS) under hypertensive conditions. To this end, rats with hypertension induced by NG-nitro-L-arginine methylester (L-NAME) or high fructose drinking (HFD), and spontaneously hypertensive rats (SHRs) were used to explore the effects/mechanisms of NPY on BP using functional, molecular, and electrophysiological approaches. The data showed that BP was elevated along with baroreceptor sensitivity dysfunction in model rats;Y1R was up-or down-regulated in the NG or NTS of male and female HFD/L-NAME groups,while Y2R was only down-regulated in the HFD groups as well as in the NG of the male L-NAME group. In SHRs,Y1R and Y2R were both down-regulated in the NTS, and not in the NG. In addition to NPY-mediated energy homeostasis, leptin-melanocortin activation may be essential for metabolic disturbance-related hypertension. We found that leptin and a-melanocyte stimulating hormone (aMSH) receptors were aberrantly down-regulated in HFD rats. In addition, a-MSH concentrations were reduced and NPY concentrations were elevated in the serum and NTS at 60 and 90 min after acute leptin infusion. Electrophysiological recordings showed that the decay time-constant and area under the curve of excitatory post-synaptic currents were decreased by Y1R activation in A-types, whereas, both were increased by Y2R activation in Ah-or C-types. These results demonstrate that sex-and afferent-specific NPY receptor expression in the baroreflex afferent pathway is likely to be a novel target for the clinical management of metabolism-related and essential hypertension.

Baroreflex Control of Heart Rate in Mice Overexpressing Human SOD1: Functional Changes in Central and Vagal Efferent Components

Excessive reactive oxygen species(ROS)(such as the superoxide radical) are commonly associated with cardiac autonomic dysfunctions. Though superoxide dismutase 1(SOD1) overexpression may protect against ROS damage to the autonomic nervous system, superoxide radical reduction may change normal physiological functions. Previously, we demonstrated that human SOD1(hSOD1) overexpression does not change baroreflex bradycardia and tachycardia but rather increases aortic depressor nerve activity in response to arterial pressure changes in C57 B6 SJL-Tg(SOD1)2 Gur/J mice. Since the baroreflex arc includes afferent, central, and efferent components, the objective of this study was to determine whether hSOD1 overexpression alters the central and vagal efferent mediation of heart rate(HR) responses. Our data indicate that SOD1 overexpression decreased the HR responses to vagal efferent nerve stimulation but did not change the HR responses to aortic depressor nerve(ADN)stimulation. Along with the previous study, we suggest that SOD1 overexpression preserves normal baroreflex function but may differentially alter the functions of the ADN, vagal efferents, and central components. While SOD1 overexpression likely enhanced ADN function and the central mediation of bradycardia, it decreased vagal efferent control of HR.

压力反射激活疗法治疗射血分数降低型心力衰竭的Meta分析

目的系统评价压力反射激活疗法(BAT)治疗射血分数降低型心力衰竭(HFrEF)的有效性和安全性。方法计算机检索PubMed、Embase、Cochrane Library、Web of Science、万方数据知识服务平台和中国知网等数据库,检索关于BAT治疗HFrEF的随机对照试验。筛选文献和偏倚风险评价后,采用RevMan 5.4软件进行Meta分析。结果最终纳入6项文献共10项研究。Meta分析结果显示:BAT组的6 min步行距离改善情况、美国纽约心脏病协会心功能分级改善情况、心力衰竭再住院次数、心力衰竭再住院持续时间均优于对照组(均P<0.05),而两组在降低全因死亡率,以及改善生活质量评分和左室射血分数方面的差异均无统计学意义(均P>0.05)。结论BAT能改善HFrEF患者的心功能和运动耐量,降低患者心力衰竭再住院风险,但仍需更多大样本的随机对照试验证实所得结论。

缺氧诱导因子-1α与阻塞性睡眠呼吸暂停相关高血压的研究进展

阻塞性睡眠呼吸暂停(OSA)是一种呼吸障碍性疾病,与顽固性高血压密切相关。OSA可引起缺氧诱导因子-1α(HIF-1α)的水平升高,并且间歇性低氧(IH)会导致HIF-α亚型失调,与OSA相关高血压相关。本研究探讨IH引起HIF-α亚型失调导致活性氧(ROS)的生成增加,进而激活化学反射、减弱压力反射并且导致内皮功能障碍影响血压调节的机制,展望HIF-1α相关抑制性药物用于治疗OSA相关高血压的前景。

黄芪对自发性高血压大鼠动脉压力反射敏感性的影响

目的:评价黄芪的降压效应及其在降压过程中对压力反射敏感性(BRS)的影响。方法:12周龄自发性高血压大鼠(SHR)19只,采用不同剂量的黄芪注射液腹腔注射给药,每天1次,共8周。并连续定时观察血压变化,8周后测定BRS,并比较用药各组与不用药组血压、BRS的差异。结果:未用药组SHR血压自第3周开始升高(P<0.01),而给药的各组SHR血压无变化;经黄芪处理后的各组SHR的BRS明显比自然饲养的SHR高(P<0.01或P<0.05)。结论:黄芪可以改善SHR的BRS。

前庭刺激对心血管自主神经调节及立位耐力的影响

目的观察前庭刺激前后被动直立位耐力试验心率、血压和压力感受器敏感性等指标的变化,了解前庭刺激对心血管自主神经调节功能及直立位耐力的影响。方法对15名男性健康志愿者在转椅刺激前、后进行被动直立位耐力检查。被动直立位耐力实验全程监测心电图和左手中指逐跳血压,在试验的第20,21,23,25,30,35,40,41,45 min测量常规血压、心率和压力感受器反射敏感性指标(BRS)。结果前庭刺激前直立位耐力检查结果均正常,刺激后有两人发生晕厥前症状;常规血压(SBP、DBP)检查在大部分实验时间无统计学差异,心率在检测的大部分时间点有统计学差异;BRS指标仅在直立位25～min段、30～min段有统计学差异,其余检测时间段没有统计学差异。结论前庭刺激可能会削弱机体心血管压力感受器反射调节功能的稳定性,造成部分志愿者直立位耐力的降低。

腺苷对颈动脉窦压力感受器反射的易化作用

在27只隔离灌流颈动脉窦区的麻醉大鼠，观察了腺苷（adenosine，Ado）对颈动脉窦压力感受器反射的影响。所得结果如下：（1）以 Ado（125μmol／L）隔离灌流大鼠左侧颈动脉窦区时，压力感受器机能曲线向左下方移位，曲线最大斜率（PS）由0．37±0．02增至0 55±0．02kPa／KPa（P＜0．001），反射性血压下降幅度（RD）由5．53±0．12增至7．76±0．36KPa；阈压（TP）、平衡压（EP）和饱和压（SP）则分别从8．60±0．27，12．53±0．30和23．69±0．15下降至5．63± 0．11kPa，10．89±0．29KPa和20．18±0．55KPa（P＜0．01－0．001 ）。其中RD，PS和TP的变化呈明显的剂量依赖性。（2）用腺苷选择性 A1受体拮抗剂（8－cyclopentyl－l，3－dipropylianthene，0．134mmol／L）预处理后，Ado的上述反射效应即被阻断。（3）先给予KATP通道阻断剂格列苯脲（glibenclamide．10μmol／L）亦可取消腺苷对压力感受器反射的影响。以上结果表明， Ado对大鼠颈动脉窦压力感受器活动有易化作用，这一作用似与腺苷A1受体介导的KATP通道开放有关。

高血压病患者压力感受器敏感性

目的探讨高血压病患者压力感受器敏感性(BRS)情况及其可能影响因素。方法用全自动生化仪测定血脂、血糖,用倾斜方法同时记录血压和心率,BRS=(最低血压时RR间期-基础RR间期)/(最低血压-基础血压),用袖带对肱动脉加压后放气,测定肱动脉内径变化率的方法代表血流介导的内皮舒张功能。结果(1)高血压病患者的BRS明显小于正常对照组[(6.9±7.3vs13.9±3.6)ms/mmHg,P<0.01],亦明显小于肾性高血压组[(6.9±7.3vs12.2±6.2)ms/mmHg,P<0.01];高血压病BRS有随着高血压分级增高而下降趋势,1级患者BRS大于3级患者[(10.2±4.0vs5.4±4.8)ms/mmHg,P<0.01],2级患者BRS大于3级患者[(7.6±2.4vs5.4±4.8)ms/mmHg,P<0.01];(2)高血压病伴高脂血症患者BRS小于高血压病不伴高脂血症组[(2.2±4.7vs7.2±6.4)ms/mmHg,P<0.01];(3)高血压病患者血管内皮舒张功能与BRS相关(r=0.565,P<0.01),肾性高血压组内皮舒张功能与BRS相关(r=0.573,P<0.05),正常对照组内皮舒张功能与BRS相关(r=0.610,P<0.05)。结论(1)BRS功能降低可能是高血压病发病原因之一;(2)降脂治疗可通过升高BRS,改善高血压病患者的预后;(3)血管内皮舒张功能与BRS有关,可通过改善血管内皮舒张功能改善BRS。