Circulating endothelial progenitor cell deficiency contributes to impaired arterial elasticity in persons of advancing age

Reduced arterial elasticity is a hallmark of ageing in healthy humans and appears to occur independently of coexisting disease processes. Endothelial-cell injury and dysfunction may be responsible for this fall in arterial elasticity. We hypothesized that circulating endothelial progenitor cells (EPCs) are involved in endothelial repair and that lack of EPCs contributes to impaired arterial elasticity. A total of 56 healthy male volunteers were divided into young (n=26) and elderly (n=30) groups. Large and small artery elasticity indices were noninvasively assessed using pulse wave analysis. The number of circulating EPCs was measured by using flow cytometry. Cells demonstrating DiI-acLDL and FITC-ulex lectin double-positive fluorescence were identified as EPCs. C1 large artery elasticity and C2 small artery elasticity indices were significantly reduced in the elderly group compared with the young group (11.73+/-1.45 vs 16.88+/-1.69 ml/mm Hg x 10, P<0.001; 8.40+/-1.45 vs 10.58+/-1.18 ml/mm Hg x 100, P<0.001, respectively). In parallel, the number of circulating EPCs was significantly reduced in the elderly group compared with the young group (0.13+/-0.02 vs 0.17+/-0.04%, P<0.05). The number of circulating EPCs correlated with C1 large and C2 small artery elasticity indices (r=0.47, P<0.01; r=0.4, P<0.01). The present findings suggest that the fall in circulating EPCs with subsequently impaired endothelial-cell repair and function contributes to reduced arterial elasticity in humans with ageing. The decrease in circulating EPCs may serve as a surrogate biologic measure of vascular function and human age.     

年龄相关的循环内皮祖细胞变化与动脉弹性关系的研究

目的　研究年龄对循环内皮祖细胞及动脉弹性的影响,探讨循环内皮祖细胞水平与动脉弹性损伤的关系。方法　56例健康男性志愿者分成青年组(n=26)和老年组(n=30)。采用桡动脉脉搏分析法无创性评价健康志愿者大动脉弹性指数(C1 )和小动脉弹性指数(C2 ), 流式细胞仪测定外周血中CD34+单个核细胞的水平,单个核细胞体外培养2周,荧光显微镜鉴定FITC UEA I和DiI acLDL双染色阳性细胞为内皮祖细胞。结果　老年组与青年组相比较,C1 和C2 明显降低[C1(11. 73±1 .45)比(16 .89±1 .69)ml/mmHg×10, P<0. 001; C2 (8 .40±1 45)比(10. 58±1 .18)ml/mmHg×100, P<0 .001 ];循环内皮祖细胞数目明显减少[ ( 0 .13±0. 02 )比( 0 .17±0. 04 )%,P<0 .05];循环内皮祖细胞水平与动脉弹性指数变化呈正相关(r=0. 47, P<0. 01;r=0 .4, P<0. 01),荧光显微镜鉴定贴壁细胞FITC UEA I和DiI acLDL双染色阳性。结论　增龄导致循环内皮祖细胞数量减少,提示血管内皮修复能力下降和功能障碍,损伤动脉弹性,循环内皮祖细胞水平有可能作为评价血管功能的替代指标。     

Validation of a new index for estimating arterial stiffness: measurement of the QPV interval by Doppler ultrasound

BACKGROUND: Pulse wave velocity (PWV), a relevant indicator of arterial stiffness, can be measured noninvasively with a variety of automatic devices, but most are complexly equipped. We developed a novel index for estimating arterial stiffness as "QPV interval," which was determined by means of surface electrocardiogram and Doppler ultrasound of the brachial artery simultaneously. HYPOTHESIS: This study aimed to validate the QPV interval as an exact and convenient index for estimation of arterial stiffness. METHODS: Forty-seven patients with untreated essential hypertension and 19 normotensive subjects were enrolled. Brachial-ankle PWV (baPWV) was measured using an automatic volume-plethysmographic apparatus, and Doppler ultrasound was implemented sequentially to measure the QPV interval in each subject. Clinical biochemistry and echocardiography were performed on the same day. RESULTS: Mean baPWV was significantly higher in hypertensive patients than in normotensive subjects (p = 0.002), whereas mean QPV interval was significantly shorter in hypertensive patients than in the normotensive group (p = 0.019). A simple regression analysis demonstrated an inverse correlation between the QPV interval and baPWV (r = -0.671, p < 0.001) in all enrolled subjects. In a stepwise regression model that adjusted for age, systolic blood pressure, and other determinants of baPWV, the negative association remained between the QPV interval and baPWV (p < 0.001). CONCLUSION: The QPV interval correlates inversely with baPWV, independent of age and other determinants of baPWV; hence, the QPV interval can serve as a simple and convenient index for assessing arterial stiffness in clinical practice.     

Radial artery compliance in response to mental stress in normotensive offspring of hypertensive parents.

OBJECTIVES: Compared to normal subjects hypertensive patients have an increased radial artery isobaric distensibility, contrasting with a decrease in elasticity of large arteries and systemic compliance. To address the question whether elasticity is increased in response to long-standing elevated blood pressure or is present at an early stage of the disease, we compared normotensive offspring of hypertensive parents with control subjects. Furthermore, enhanced sympathetic response to mental stress was demonstrated in individuals predisposed to hypertension and might contribute to the elevation of blood pressure via a peripheral mechanism. Thus, an abnormal vasoconstrictive response of the radial artery to psychological stress was sought in these subjects. DESIGN: The geometry and the elastic porperties of the radial artery were assessed in normotensive offspring of hypertensive and normotensiven parents at baseline and during mental stress. METHODS: A high-precision echo-tracking ultrasound device was combined with photoplethysmography for continuous measurement of radial artery diameter and isobaric distensibility in 18 normotensive offspring of parents with essential hypertension and 18 control subjects under resting conditions and during a 3-minute mental stress test. RESULTS: Baseline arterial distensibility and compliance were comparable in offspring of hypertensive and normotensive parents. During mental stress, blood pressure and heart rate increased similarly in both groups. Adrenergic activation did not alter the elastic properties of the radial artery in the individuals with a genetic predisposition to essential hypertension. CONCLUSIONS: There was no alteration in elastic properties of the radial artery in normotensiven individuals at genetic risk to develop arterial hypertension. Furthermore, mental stress did not abnormally increase the vascular tone of this medium-sized muscular artery in these subjects as compared to controls. This indicates that functional and/or structural vascular alterations do not precede a distinct rise in blood pressure or abnormal blood pressure reactivity in subjects prone to develop essential hypertension.     

Impaired arterial elasticity in young patients with white-coat hypertension

BACKGROUND: Conflict still exists over whether patients with white-coat hypertension are at increased risk of developing target organ damage compared with normotensive individuals. METHODS: We studied vascular distensibility in 117 young-to-middle age patients with white-coat hypertension, 174 patients with sustained hypertension, and 51 normotensive controls. To obtain a measure of compliance, a model was used that divides the total systemic compliance into large artery (C1) and small artery (C2) compliance. With this aim, radial arterial pulse waves were recorded with a tonometer sensor array by means of an HDI CR2000 device (Eagan, Minnesota, USA). Moreover, pulse wave velocity and the augmentation index were measured using the Specaway DAT system (St Pauls, Sydney, Australia). RESULTS: Patients with sustained hypertension had a greater body mass index than patients with white-coat hypertension (P=0.04) or the normotensive individuals (P=0.01). C1 and C2 were decreased in the two hypertensive groups as compared with those in the normotensive group (P=0.0002 and 0.03, respectively, versus sustained hypertension; P=0.00007 and 0.0004, respectively, versus white-coat hypertension). Pulse wave velocity and aortic augmentation index were increased in the white-coat hypertension patients compared with the normotensive individuals (P=0.02 and 0.004, respectively). Aortic augmentation index (P=0.008) but not pulse wave velocity was increased in the sustained hypertensive patients compared with that in the normotensive individuals. All indexes of arterial distensibility were similar in the two hypertensive groups. CONCLUSIONS: Indexes of arterial distensibility are impaired in the white-coat hypertensive group and similar to those in the sustained hypertensive group, indicating that early changes in the arterial wall can occur in white-coat hypertension. This may account for the higher risk of stroke that has been described in this condition.     

高血压不同部位大动脉缓冲功能不均一性的临床研究

目的：研究正常人和高血压患者不同部位动脉缓冲功能的变化。方法：对１２０例正常人和２０５例原发性高血压患者应用动脉搏波速度（Ｐｕｌｓｅ ｗａｖｅ ｖｅｌｏｃｉｔｙＰＷＶ）测定仪进行检测。颈动脉－股动脉ＰＷＶ（ＣＦＰＷＶ）、肱动脉－找动脉ＰＷＶ（ＢＲＰＷＶ）和股动脉－足背动脉ＰＷＶ（ＦＴＰＷＶ）分别为反映大动脉和中等动脉扩张性（Ｄｉｓｔｅｎｓｉｂｉｌｉｔｙ）的参数。并能敏感反映动脉缓冲功能的改变。结果：无论正常人还是高血压患者,ＣＦＰＷＶ与年龄和收缩压成正相关关系（Ｐ均小于０．００１）,而ＢＲＰＷＶ和ＦＴＰＷＶ并不随年龄和收缩压的改变而改变。结论：正常人和高血压患者不同部位动脉节段的缓冲功能发生不同的变化,大动脉扩张性降低,中等动脉无明显变化。对大动脉缓冲功能变化的早期检测和有效治疗具有重要的临床价值。     

RADIAL ARTERY COMPLIANCE IN RESPONSE TO MENTAL STRESS IN NORMOTENSIVE OFFSPRING OF HYPERTENSIVE PARENTS

Objectives: Compared to normal subjects hypertensive patients have an increased radial artery isobaric distensibility, contrasting with a decrease in elasticity of large arteries and systemic compliance. To address the question whether elasticity is increased in response to long-standing elevated blood pressure or is present at an early stage of the disease, we compared normotensive offspring of hypertensive parents with control subjects. Furthermore, enhanced sympathetic response to mental stress was demonstrated in individuals predisposed to hypertension and might contribute to the elevation of blood pressure via a peripheral mechanism. Thus, anabnormal vasoconstrictive response of the radial artery to psychological stress was sought in these subjects.

Design:The geometry and the elastic porperties of the radial artery were assessed in normotensive offspring of hypertensive and normotensiven parents at baseline and during mental stress.

Methods:A high-precision echo-tracking ultrasound device was combined with photoplethysmography for continuous measurement of radial artery diameter and isobaric distensibility in 18 normotensive offspring of parents with essential hypertension and 18 control subjects under resting conditions and during a 3-minute mental stress test.

Results: Baseline arterial distensibility and compliance were comparable in offspringof hypertensive and normotensive parents. During mental stress, blood pressure and heart rate increased similarly in both groups. Adrenergic activation did not alter the elastic properties of the radial artery in the individuals with a genetic predisposition to essential hypertension.

Conclusions:There was no alteration in elastic properties of the radial artery in normotensiven individuals at genetic risk to develop arterial hypertension. Furthermore, mental stress did not abnormally increase the vascular tone of this medium-sized muscular artery in these subjects as compared to controls. This indicates that functional and/or structural vascular alterations do not precede a distinct rise in blood pressure or abnormal blood pressure reactivity in subjects prone to develop essential hypertension.     

Family history of hypertension and arterial elasticity characteristics in healthy young people

Family history of hypertension is a primary predictor of high blood pressure (BP). This study attempted to determine whether there is a gradual increase in BP and an early change in arterial elasticity characteristics between young healthy individuals with or without a family history of hypertension and whether or not this increase is apparent in males as well as in females. A total of 270 normotensive healthy individuals (112 men and 158 women, aged 16 to 30 years) with or without a family history of hypertension, participated in conventional BP measurement and completed questionnaires covering basic information and a detailed family history of cardiovascular disease. Large arterial (capacitive) compliance (C1) and small arterial (oscillatory or reflective) compliance (C2) were derived from HDI/PulseWave CR-2000 (Hypertension Diagnostics, Minneapolis, USA). Based on family history information about parents and grandparents, three groups were formed: subjects with at least one hypertensive parent (group A), subjects with only hypertensive grandparents (group B), and subjects with normotensive parents and grandparents (group C). Men in group A had lower C1 and C2 along with higher systolic BP (SBP), diastolic BP (DBP), and heart rate than men in group C. Those in group B had intermediate C1, C2 and BP levels. C1 had a linear relationship with SBP, DBP, and heart rate. In the logistic regression model of family history of hypertension, C2 was lower in young normotensive males with parental hypertension (B = -0.315, exp B = 0.73, p = 0.03), independently of SBP, DBP, and heart rate. Among females, subjects with parental hypertension had higher systolic, mean arterial pressure, and pulse pressure (p < 0.05), and there were no significant differences in C1 and C2 between those with and those without parental hypertension. In conclusion, compared with normotensive offspring of normotensive parents, normotensive offspring of hypertensive parents had increased BP and impaired arterial properties, namely large and small arterial compliance as measured noninvasively by HDI. These differences were exhibited conspicuously in men but not in women. Alteration in arterial function in young non-hypertensive subjects may be a risk factor for hypertension and may contribute to the progression to hypertension later in life.     

Increased circulating CD31+/CD42- microparticles are associated with impaired systemic artery elasticity in healthy subjects

BACKGROUND: Impaired artery elasticity has been found in various pathological conditions related to endothelial dysfunction. Recently, CD31+/CD42- microparticles (MPs) emerged as a marker of endothelial injury. Whether CD31+/CD42- MPs, generated under physiological conditions, are correlated with artery properties has not been reported. METHODS: We evaluated brachia-ankle pulse-wave velocity (baPWV) (n = 76) and C1 large-artery and C2 small-artery elasticity indices (n = 56), using noninvasive devices for pulse-wave analysis in a group of healthy persons. The number of circulating CD31+/CD427- MPs (n = 76) was measured by flow cytometric analysis. RESULTS: Circulating CD31+/CD42- MPs were positively correlated with values of baPWV (r = 0.371, P = .008) and with C1 large-artery and C2 small-artery elasticity indices (r = -0.294, P = .037; and r = -0.310, P = .027, respectively). Multivariate analysis identified CD31+/CD42- MPs as potent contributors to the development of impaired systemic artery elasticity. CONCLUSIONS: The level of circulating CD31+/CD42- MPs, an important biomarker of dysfunctional endothelium and vascular injury, is closely associated with impaired systemic artery elasticity in healthy subjects. The present study suggests that CD31+/CD42- MPs may be a novel surrogate marker for the clinical evaluation of vascular damage.     

冠心病患者内皮祖细胞与动脉弹性相关性及缬沙坦干预研究

目的探讨冠状动脉粥样硬化性心脏病(coronary heart disease,CHD)患者内皮祖细胞(endothelial progenitor cell,EPCs)数量及动脉弹性指数之间的相关性,以及缬沙坦干预后EPCs水平和动脉弹性指数变化。方法冠状动脉造影检查确诊的冠心病患者60例为CHD组,同期排除冠心病的门诊健康体检者60例为对照组。两组患者采集外周血用密度梯度离心法获取单个核细胞,接种在人纤维连接蛋白包被的培养板,培养贴壁后进行细胞化学分析。激光共聚焦显微镜鉴定FITC-UEA-I和DiI-acLDL双染色阳性细胞为正在分化的EPC。进行EPCs水平测定。动脉弹性功能检测仪测定患者的大、小动脉弹性指数(C1、C2)。CHD组患者术后缬沙坦80mg/天干预12、24周后再次检测EPCs水平和动脉弹性指数。结果CHD组EPCs数量、C1、C2分别为32.8±6.4 EPCs/×200视野、9.82±1.54、3.67±0.87,对照组为61.6±9.5 EPCs/×200视野、15.3±2.52、7.51±2.03,两组差异有显著统计学意义(P<0.01);CHD组动脉弹性功能指数与EPCs水平呈正相关(r值分别为0.94、0.98,均P<0.01)。CHD组患者缬沙坦80mg/天干预12、24周后EPCs数量明显增加(37.7±7.98 vs 50.80±8.10,P<0.01),动脉弹性指数改善(C1:10.6±1.98 vs 12.55±2.43,C2:4.37±1.03 vs 5.77±1.99,均P<0.01),差异有显著统计学意义。结论CHD患者EPCs水平减低和动脉弹性指数下降是冠心病发病的独立危险因素之一,且两者之间呈正相关。CHD患者缬沙坦80mg/天干预12、24周后明显提高EPCs数量和动脉弹性指数。     

高血压病患者胰岛素抵抗与动脉弹性指数的相关性

目的: 分析动脉弹性指数与高血压病患者胰岛素抵抗相关因素之间的相关性。方法: 测定112例高血压病患者动脉弹性指数与血压、糖脂代谢及红细胞内Mg2+,Ca2+离子等指标,并对各项指标进行相关及回归分析。结果: 高血压病患者大动脉弹性指数（C1）和小动脉弹性指数（C2）与胰岛素敏感指数（ISI）呈正相关,它们均与收缩压、舒张压及平均动脉压、体质量指数、血清三酰甘油和红细胞内Mg2+呈负相关。结论: 高血压病患者胰岛素抵抗相关因素与动脉弹性指数之间有相关性。     

Berberine-induced mobilization of circulating endothelial progenitor cells improves human small artery elasticity

Berberine (BR) has been proved to promote endothelial function. However, the exact mechanisms underlying the effect of BR on endothelial function are not completely clear. It has been demonstrated that endothelial progenitor cells (EPCs) contribute to improvement of endothelial function and C2 small artery elasticity index is a surrogate parameter for the clinical evaluation of endothelial function. We hypothesized that BR-induced mobilization of circulating EPCs is associated with BR-related improvement of endothelial function. To address this assumption, 15 healthy volunteers were recruited and received BR 0.4 g three times per day for 30 days. The number of circulating CD34/KDR double-positive cells as well as C1 large and C2 small artery elasticity indices were evaluated before and after BR therapy. The number of CD34/KDR double-positive EPCs increased significantly after BR treatment (0.030+/-0.020% vs 0.017+/-0.010%, P<0.01). After 30-day BR therapy C2 increased significantly (6.21+/-2.80 ml per mm Hg x 100 vs 4.06+/-2.67 ml per mm Hg x 100, P<0.01) and C1 remained unchanged (10.79+/-3.27 ml per mm Hg x 10 vs 10.06+/-2.08 ml per mm Hg x 10, P>0.05). The increment of CD34/KDR double-positive EPCs was positively correlated with the increment of C2 (r=0.68, P<0.01). We concluded that BR-induced mobilization of circulating EPCs contributes to improvement of small artery elasticity in healthy persons.     

Relationship between arterial elasticity indices and carotid artery intima-media thickness

Functional and structural changes of the arterial wall appear to serve as early hallmarks of the hypertensive disease process. Structural vascular changes can be studied by the determination of the intima-media wall thickness (IMT) at the carotid artery. The elastic behavior of the proximal and distal parts of the arterial tree can be assessed from noninvasively recorded radial artery waveforms. The aim of the study was to compare large (proximal, C1) and small (distal, C2) artery elasticity indices in two age-matched study groups with high- and low-normal blood pressure (BP) and to assess the relation between elasticity indices and IMT. A total number of 22 subjects with high-normal BP (40 +/- 2 years; BP, 147 +/- 2.5/84 +/- 1.5 mm Hg) and 22 matched controls with low-normal BP (40 +/- 2 years; BP, 123 +/- 1.9/69 +/- 1.5 mm Hg) were enrolled. The IMT was echographically determined at the common carotid artery by the leading-edge technique. Large artery (C1) and small artery (C2) elasticity indices were calculated from a third-order, four-element model of the arterial circulation. In the group with high-normal BP large and small artery elasticity indices were significantly decreased versus controls with low-normal BP (C1: 1.63 +/- 0.08 v 1.99 +/- 0.09 mL/mm Hg, P < .01; C2: 0.059 +/- 0.005 v 0.076 +/- 0.007 mL/ mm Hg, P < .05) and IMT increased significantly (0.607 +/- 0.039 v 0.516 +/- 0.027 mm, P < .05). Moreover, there was an inverse relationship between IMT and small artery elasticity index (r = -0.60, P = .004). In subjects with a high-normal BP there is already a change in the IMT of the carotid artery versus normotension. The IMT is related to the small artery elasticity index (C2).     

Arterial elasticity among normotensive subjects and treated and untreated hypertensive subjects

OBJECTIVE: The aim of this study was to determine arterial elasticity in normotensive and hypertensive individuals. BACKGROUND: In addition to blood pressure, other parameters serve as markers for vascular disease. Arterial elasticity is one parameter that can be determined by a modified Windkessel model of the circulation. This model estimates, from a computerized pulse contour analysis, the proximal (capacitive) elasticity of the large arteries and the distal (reflective) elasticity of the small arteries. METHODS: A prospective, multi-center, controlled clinical study evaluated large-artery and small-artery elasticity indices in four groups: (1) normotensives without a family history of hypertension; (2) normotensives with a family history of hypertension; (3) treated and controlled hypertensives; and (4) untreated and uncontrolled hypertensives. Blood pressure, using a mercury manometer, and arterial elasticity, using a CVProfilor DO-2020 CardioVascular Profiling System (Hypertension Diagnostics, Inc., Eagan, MN, USA), were measured supine in triplicate 3 min apart in a randomized sequence. RESULTS: There were 212 evaluable subjects of mean age 46 years; 57% were women, 51% Caucasian and 33% African-American. Comparing normotensives without a family history and untreated hypertensives, both large-artery and small-artery elasticity indices were significantly different (P < 0.0001). After controlling for age and body surface area, a significant linear trend (P = 0.0001) across the four groups was detected for both large- and small-artery elasticity indices. CONCLUSION: As the hypertension status worsened, large- and small-artery elasticity indices decreased, suggesting a potential for the diagnostic use of arterial elasticity determinations.     

Postprandial hyperinsulinemia in patients with mild essential hypertension

Glucose tolerance tests and diurnal profiles of glucose, insulin, free fatty acids, serum triglycerides, total and high-density lipoprotein cholesterol levels were performed in 8 male patients with mild essential hypertension as well as in 20 normotensive subjects. Although glucose tolerance and postprandial glucose levels appeared equal in both groups, the insulin response after a glucose load and after each meal was significantly increased in hypertensive subjects as compared with the controls (p less than 0.01). The levels of free fatty acids were higher in the postabsorptive phase of patients with hypertension in comparison to normotensive subjects, but decreased markedly when plasma insulin levels rose after meals. In both subject groups serum triglyceride levels showed the typical postprandial increase. Total and high-density lipoprotein cholesterol levels showed neither diurnal variations nor differences between hypertensive subjects and normotensive controls. Postprandial hyperinsulinemia in patients with mild essential hypertension possibly may provoke lipid accumulation in the arterial wall and therefore may be a relevant risk factor for atherosclerosis in these subjects.     

Arterial elasticity identified by pulse wave analysis and its relation to endothelial function in patients with coronary artery disease

Patients with coronary artery disease (CAD) have impaired endothelial function. Arterial elasticity is modulated by endothelial function. The association between arterial elasticity and endothelial function has not been reported in patients with CAD. The present study was designed to investigate whether endothelial dysfunction contributes to impaired arterial elasticity. Thirty patients with CAD and 30 control subjects were recruited. Large and small artery elasticity indices were non-invasively assessed using pulse wave analysis. Brachial artery endothelium-dependent and -independent function were assessed by vascular response to flow-mediated vasodilation (FMD) and sublingual nitroglyceride (NTG), respectively. C1 large artery elasticity index was not different in the CAD group compared with the control group. However, C2 small artery elasticity index was significantly reduced in the CAD group compared with the control group. Flow-mediated vasodilation (FMD) was also impaired in the CAD group compared with the control group. Flow-mediated vasodilation (FMD) in the brachial artery correlated with C2 small arterial elasticity index. But NTG-mediated brachial artery vasodilation was similar between the two groups. The present findings suggest that the patients with CAD have reduced C2 small arterial elasticity index and impaired FMD. Endothelial dysfunction is involved in diminished arterial elasticity, suggesting that C2 small arterial elasticity index is a novel surrogate measure for the clinical evaluation of endothelial function.     

Vascular endothelial growth factor polymorphism (–460 T/C) is related to hypertension-associated chronic kidney disease

Our aim was to characterize the endothelial progenitor cells (EPCs) in normotensive controls and treated hypertensive individuals within the vascular endothelial growth factor (VEGF) –460 C/T polymorphism as well as to investigate whether this polymorphism predisposes to hypertension-related chronic kidney disease. The hypertensive patients bearing the TT genotype had the highest levels of immature EPC with the following phenotypes: CD34⁺, CD34⁺CD45^dim, CD34⁺CD133⁺CD45^dim. The study showed the estimated glomerular filtration rate values significantly lower and creatinine and BUN parameters higher among the TT hypertensive patients. We presume that the highest mobilization of EPCs from bone marrow may signalize more severe renal hypertension-related complications in the VEGF –460 TT genotype.     

Arterial elasticity and erectile dysfunction in hypertensive men

Erectile dysfunction is a common symptom among hypertensive patients that impairs quality of life and adherence to antihypertensive pharmacologic therapy. It is also associated with cardiovascular risk factors and disease. The Sexual Health Inventory in Men (SHIM) was administered to 105 ambulatory hypertensive patients, and large and small artery elasticity indices were measured. Each variable was examined in a simple linear regression model or 1-way analysis of variance model to determine each variable's relationship with the SHIM score. Variables that were significantly associated with the SHIM score in the univariate models included age, duration of hypertension, peripheral vascular disease, and small artery elasticity. Large artery elasticity was not significantly associated with the SHIM score. In the multivariate model, age, hypertension duration, and peripheral vascular disease were associated with a lower SHIM score. This study demonstrates a relationship between erectile dysfunction and reduced artery elasticity.     

Association Between Increased Plasma Levels of Aldosterone and Decreased Systemic Arterial Compliance in Subjects With Essential Hypertension

We previously observed that, in subjects with essential hypertension, acute ouabain constricts the brachial artery diameter in the presence of spironolactone treatment, a finding that is not observed in the absence of aldosterone antagonist and therefore suggests a specific effect of aldosterone on the arterial wall. To evaluate whether aldosterone excess may contribute to modulate arterial function, we investigated 56 patients with sustained essential hypertension in comparison with 36 normotensive controls. Systemic arterial compliance was measured from intraarterial blood pressure and cardiac output measurements using a classical Windkessel model to determine the elasticity of the proximal arterial tree. Radial artery compliance was determined using a previously described echo tracking technique. In hypertensive, but not in normotensive, subjects, systemic arterial compliance was strongly and negatively correlated with plasma aldosterone. The correlation was observed even after adjustment for age and blood pressure. Plasma potassium and renin activity did not interfere in the correlation. Acute administration of diltiazem did not change systemic compliance but significantly decreased plasma aldosterone, suggesting that, in the presence of calcium blockade, the same compliance was achieved for a lower plasma aldosterone level. Taken together, these findings strongly suggest that significant interactions exist between aldosterone and central conduit arteries and that aldosterone might modulate arterial function in subjects with essential hypertension.     

Evidence using human arterial tissue for a circulating vascular sensitizing agent in essential hypertension

We studied the effect of plasma from 12 patients with essential hypertension and 12 normotensive subjects on the contractile response to norepinephrine in human isolated arterial spiral strips. Human mesenteric and uterine arteries were obtained during abdominal surgery; they were cut into spiral strips and set up in isolated organ baths. After the equilibration period, arterial strips were incubated for 20 min in plasma from either normotensive subjects or hypertensive patients, and the contractile responses to norepinephrine (2.96 X 10(-7) M) were recorded. Plasma from hypertensive subjects significantly increased the contractile response to norepinephrine by 25.8% (P less than 0.02). Plasma from normotensive subjects did not increase the contractile response to the pressor agent (-3.2%; P = NS). The mean change in contractile response to norepinephrine in the presence of plasma from hypertensive patients was significantly higher than that after incubation of the human arterial strips in plasma from normotensive subjects (P less than 0.02). When both groups were considered as a whole, there was a significant correlation between diastolic pressure and the change in the contractile response to norepinephrine (r = 0.52; P less than 0.01). These results suggest the existence of a circulating vascular sensitizing substance in patients with essential hypertension.