Blockade of the renin-angiotensin system increases adiponectin concentrations in patients with essential hypertension

Adiponectin, an adipocyte-derived protein, has been suggested to play an important role in insulin sensitivity. We examined the association between insulin sensitivity (M value) evaluated by the euglycemic-hyperinsulinemic glucose clamp and adiponectin concentrations in 30 essential hypertensives (EHT) and 20 normotensives (NT) and investigated the effect of blockade of the renin-angiotensin system (RAS) on adiponectin concentrations. EHT were divided into 12 insulin-resistant EHT (EHT-R) and 18 non-insulin-resistant EHT (EHT-N) using mean-1 SD of the M value in NT. There were no intergroup differences in age, gender, and body mass index (BMI). EHT-R had significantly higher levels of insulin and triglyceride and lower levels of adiponectin than did NT and EHT-N. EHT-R had higher levels of free fatty acid and lower levels of high-density lipoprotein (HDL) cholesterol than did EHT-N. Adiponectin concentrations were positively correlated with M value and HDL cholesterol and negatively correlated with BMI, insulin, free fatty acid, and triglyceride but not with blood pressure. M value, BMI, and HDL cholesterol were independent determinants of adiponectin concentrations in multiple and stepwise regression analyses. Sixteen EHT were treated with an angiotensin-converting enzyme inhibitor (temocapril, 4 mg/d; n=9) or an angiotensin II receptor blocker (candesartan, 8 mg/d; n=7) for 2 weeks. Treatment with temocapril or candesartan significantly decreased blood pressure and increased M value and adiponectin concentrations but did not affect BMI and HDL cholesterol. These results suggest that hypoadiponectinemia is related to insulin resistance in essential hypertension and that RAS blockade increases adiponectin concentrations with improvement in insulin sensitivity.     

Role of adiponectin in insulin-resistant hypertension and atherosclerosis.

Insulin resistance is one of the major risk factors associated with development of hypertension and atherosclerosis. Recent studies have shown that adiponectin, an adipocyte-derived hormone, may be involved in insulin resistance and development of atherosclerosis in diabetes patients. The aim of this study was to examine adiponectin levels in patients with essential hypertension to determine the relationships between adiponectin levels and insulin sensitivity and to examine the relationship of adiponectin with pulse wave velocity (PWV) in a general population based on the results of an epidemiological survey in Japan. In a clinical study, 20 normotensives (NT) and 30 non-treated essential hypertensives (EHT) were hospitalized, and euglycemic hyperinsulinemic glucose clamp (GC) was performed to evaluate insulin sensitivity defined as M value. EHT were divided into insulin-resistant EHT (EHT-R) and insulin-nonresistant EHT (EHT-N) according to the mean -1 SD of the M value of NT as a cut-off point. Fasting plasma glucose (FPG), immunoreactive insulin (IRI), and adiponectin concentrations were measured. There were no significant differences in body mass index (BMI) or FPG among the NT, EHT-N, and EHT-R groups. The M value and adiponectin concentration in EHT-R were significantly lower than those in the NT or EHT-N. The IRI level in the EHT-R was significantly higher than those in the other groups. A positive correlation between adiponectin concentration and M value was found in all subjects, and adiponectin concentration and M value were found to be significant determinants of each other in multiple regression analysis. In an epidemiological study, we studied 391 male inhabitants of rural communities in Hokkaido, Japan. Systolic blood pressure (SBP), BMI, FPG, IRI, and adiponectin were measured in all subjects early in the morning. Homeostasis model assessment (HOMA) values were calculated as an index of insulin sensitivity, and PWV was used as an index of atherosclerosis. A negative correlation between HOMA values and adiponectin concentration was found in all of the subjects. Multiple regression analysis revealed that adiponectin was a significant determinant for PWV in subjects less than 70 years of age. The results of the clinical study indicate that EHT-R had not only hyperinsulinemia but also a low concentration of adiponectin. The results of multiple regression analysis for determinants of degree of PWV using data obtained in the epidemiological study suggest that adiponectin plays a role in antiatherosclerosis, partly through improvement of insulin resistance.     

Circulating resistin levels in essential hypertension

OBJECTIVE: Resistin, a novel cysteine-rich protein secreted by adipocytes, has been proposed to serve as a link between obesity and insulin resistance in rodents, but this has remained controversial. Most of the data obtained in previous studies are restricted to mRNA levels in tissues. DESIGN AND PATIENTS: We examined the association between insulin resistance and circulating protein levels of resistin in 33 essential hypertensive patients (EHT) and 18 normotensive subjects (NT). Insulin sensitivity (M-value) was evaluated by the euglycaemic hyperinsulinaemic glucose clamp technique. RESULTS: Using a cutoff point of mean - 1 SD of the M-value in the NT, the EHT were divided into two groups: one group of 12 insulin-resistant patients (EHT-R) and one group of 21 noninsulin-resistant patients (EHT-N). There were no intergroup differences in age, gender, body mass index (BMI; range: 20.1-30.4 kg/m2), fasting glucose and total cholesterol. The EHT-R had significantly higher levels of fasting insulin and triglyceride than did the NT and the EHT-N. The EHT-R had higher levels of free fatty acid and lower levels of high-density lipoprotein cholesterol than did the EHT-N. The M-value was negatively correlated with fasting insulin, free fatty acid, and triglyceride. Circulating resistin levels were not significantly different among the three groups and were not correlated with the M-value, BMI, blood pressure, or lipid variables. CONCLUSIONS: Our results suggest that circulating resistin levels are not related to insulin resistance, at least in patients with essential hypertension, although disturbance of lipid metabolism may be associated with insulin resistance.     

Enhanced blood pressure response to isometric handgrip exercise in patients with essential hypertension: effects of propranolol and prazosin

To elucidate whether a difference exists in blood pressure (BP) elevation during isometric handgrip exercise (IHG) between essential hypertensives (EHT) and normotensives (NT), IHG was carried out in 12 NT and 46 EHT under constant sodium intake using a new instrument. The acute effects of propranolol and prazosin on IHG were also examined in EHT. The change in systolic BP (delta SBP) during IHG in EHT, delta SBP = 61 +/- 21 mmHg, was markedly greater than that in NT, delta SBP = 28 +/- 4 mmHg. Among EHT, delta BP increased with increasing severity of hypertension. Neither the changes in plasma norepinephrine nor in epinephrine during IHG showed significant differences between EHT and NT. The pressor response during IHG could not be suppressed by propranolol, but about 30% suppression of BP was observed during IHG with prazosin. It is concluded from these findings that EHT have an exaggerated BP response to IHG that is due to increased post-junctional alpha 1-adrenoceptors.     

The pathophysiological role of renal dopaminergic activity in patients with essential hypertension

To evaluate the role of the renal dopaminergic system on renal water-sodium metabolism patients with essential hypertension (EHT), urinary excretion of dopamine, urinary excretion of sodium (UNaV) and fractional excretion of sodium (FENa) were all investigated before and after the administration of dopamine (3 micrograms/kg/min, intravenous infusion for 60 minutes), dopamine antagonist, metoclopramide (8 mg/m2 BSA, intravenous injection) or mild sodium loading in both normotensive subjects and benign EHT. In the basal values, no significant difference in urinary excretion of free (u-fDA), conjugated (u-cDA) or total dopamine (u-tDA) was found between normotensives and hypertensives. However, low renin EHT showed a pronounced reduction in u-fDA compared with normotensis subject and (NT) normal renin EHT. In this study, a significant reduction of u-cDA and of u-tDA was also found in those patients with low renin essential hypertension. In the normotensive and essential hypertensive groups UNaV or FENa showed a positive correlation with u-fDA (measured simultaneously), but not with u-tDA or u-cDA. The regression line between u-fDA and UNaV or FENa in EHT was shifted towards a lower u-fDA level than in NT. UNaV and FENa were increased by dopamine infusion and were decreased by metoclopramide injection in both NT and EHT. Changes of UNaV and FENa following dopamine or metoclopramide, showed a negative correlation with u-fDA measured immediately before the administration of these drugs. The enhanced natriuretic response to infused dopamine and the attenuated antinatriuretic response to injected metoclopramide were significant in low renin EHT, when compared with NT or normal renin EHT patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

High Plasma Immunoreactive Leptin Level in Essential Hypertension

Insulin resistance, the most important factor in metabolic syndrome X, has been considered to raise blood pressure. Recently it was reported that insulin resistance was related to an elevated plasma level of leptin, which is an adipocyte-specific ob gene product and which plays a role in food intake suppression, thermogenesis, and energy expenditure through the activation of the hypothalamus. However there are no reports that deal with the relationship of insulin resistance to plasma leptin and blood pressure.To evaluate the role of leptin in essential hypertensives, two groups of subjects who were carefully matched for body mass index (BMI) were studied; 22 normotensives (NT, age: 46.5 ± 2.6 years, BMI: 23.9 ± 0.4 kg/m², male/female: 14/8) and 45 mild-to-moderate essential hypertensives (EHT, age: 51.9 ± 2.0 years, BMI: 24.5 ± 0.4 kg/m², male/female: 21/24). We applied the euglycemic hyperinsulinemic glucose clamp technique to all subjects and insulin sensitivity was evaluated as the M value. EHT showed a significantly lower M value (160.2 ± 7.4 v 184.3 ± 7.3 mg/m²/min, P < .05) and higher basal plasma immunoreactive leptin level (7.6 ± 0.8 v 5.0 ± 0.8 ng/mL, P < .05) than NT, despite the fact that there was no significant difference between NT and EHT in age, gender, or BMI. The relationship between mean blood pressure and leptin showed a significant positive correlation in all of the subjects (r = 0.31, P < .05), suggesting that leptin may be related to a pathophysiology of essential hypertension.     

高血压遗传史与胰岛素抵抗，高血压的关联

目的 探讨高血压遗传史对第二、三代直系亲属血压水平,胰岛素抵抗及致动脉粥样硬化危险因素的影响。方法 对象为高血压家族史阳性病例187人,高血压家族史阴性99人及他们的配偶子女286家858人,指标包括血压、血糖、总胆固醇、甘油三脂、高密胆固醇、纤维蛋白原、胰岛素敏感指数。结果 调整年龄、性别影响后,高血压家族史阳性第二代高血压、血压正常者之胰岛素敏感指数相似,但均相当于高血压家族史阴性第二代非高血压的2／3。高血压家族史阳性的第二代高血压,血压正常者组的FSG、TC、TG、FB均高于而HDL－c低于后者。第三代子女间血压、TC、TG、FSG、HDL－c趋势与第二代结果相似,但胰岛素敏感指数仅为家族史阴性组的4／5。结论 高血压遗传因素可影响第二代及第三代子女,不管遗传或不遗传高血压,但毫无例外地遗传胰岛素抵抗及相关的代谢,表明胰岛素抵抗是高血压遗传因素的主要内容;胰岛素抵抗是否产生高血压尚必须有其他辅助条件或环境因素。     

Changes in 24 Hour Blood Pressure and in Cardiac and Vascular Structure in Normotensive Subjects with Parental Hypertension

Subjects with family history of hypertension represent a suitable model to investigate the mechanisms responsible for early cardiovascular structural and functional changes occurring in essential hypertension. In our study we have addressed the factors involved in determining the mild elevation in office blood pressure frequently observed in normotensive subjects with hypertensive parents. In 15 normotensive subjects with both parents hypertensive (FH++) and in 15 normotensive subjects with one parent hypertensive (FH+?) we found no evidence of a hyperreactivity to stress as compared to the responses of 15 normotensive subjects with no parental hypertension (FH–). On the contrary FH++ subjects were characterized by a significant although mild increase in their blood pressure values recorded either at rest and in ambulatory conditions over the 24 hours, including night sleep. FH++ and FH+? subjects also showed a greater left ventricular mass thickness and a greater minimal forearm vascular resistence than FH subjects. Thus, the elevation in blood pressure found in the pre-hypertensive stage in subjects with positive family history for hypertension does not reflect a hyperreactivity to the stress associated with physician's visit but indicates an early and persistent blood pressure elevation. This blood pressure elevation is accompanied by early cardiovascular structural changes which may indicate that these subjects are exposed to a higher risk even before developing overt hypertension.     

Early 24-hour blood pressure elevation in normotensive subjects with parental hypertension

Subjects with a family history of parental hypertension are reported to have a slightly higher office blood pressure in the prehypertensive stage. Whether this reflects a hyperreactivity to blood pressure measurement or a more permanent blood pressure elevation, however, is not known. In the present study, blood pressure was measured in 15 normotensive subjects whose parents are both hypertensive (FH++), 15 normotensive subjects with one hypertensive parent (FH(+)-), and 15 normotensive subjects whose parents are not hypertensive (FH--); among the three groups, subjects were matched for age, sex, and body mass index. The measurements were made in the office during a variety of laboratory stressors and during a prolonged resting period, and for a 24-hour period (ambulatory blood pressure monitoring). Office blood pressure was higher in the FH++ group than in the FH-- group (p less than 0.05). The pressor responses to laboratory stressors were similar in the two groups, but the FH++ group had higher prolonged resting and 24-hour blood pressure than the FH-- group; the difference was always significant (p less than 0.05) for systolic blood pressure. The FH++ group also had a greater left ventricular mass index (on echocardiographic examination) than the FH-- group (p less than 0.01). The blood pressure values and echocardiographic values of the FH(+)- group tended to be between those of the other two groups. Thus, the higher blood pressure shown by individuals in the prehypertensive stage with a family history of parental hypertension does not reflect a hyperreactivity to stress but an early permanent blood pressure elevation.(ABSTRACT TRUNCATED AT 250 WORDS)     

AT_1R基因多态性对血压的影响

目的 检测血管紧张素Ⅱ的Ⅰ型受体(AT_1R)C1166等位基因在正常人和原发性高血压(EH)患者中的频率,并研究中国汉族人AT_1R基因多态性与原发性高血压的关系.方法 测定120例汉族原发性高血压病人和86个汉族正常人的血压、体重指数、空腹血糖及血胆固醇和甘油三酯浓度.用盐析法提取外周血白细胞DNA,用PCR加上限制性酶切方法检测AT_1R的C1166位基因突变.结果 高血压组除收缩压、舒张压显著高于对照组外,其它临床指标如体重指数、空腹血糖及血脂水平两组间无显著差异;EH患者AT_1R基因AC基因型频率比正常对照组高(0.081vs 0.058,P<0.01),C1166等位基因频率EH组高于正常对照组(0.091vs 0.029,P<0.05);两组中均未发现CC纯合子基因型;进行性别分组后,发现在女性EH患者C1166等位基因频率高于女性正常对照组(0.125 vs 0. 031,P<0.05),在男性EH患者C166频率与男性正常对照组无显著差异(0.072vs O.028,P>0.05);将EH组分为有、无高血压家族史两组,发现有高血压家族史的EH患者C1166频率高于无家族史EH患者(0.123 vs 0.035,P<0.05).结论 在中国汉族人群中,AT_1R基因多态性与原发性高血压有关;C1166等位基因可能是一个高血压的易感基因,并与有家族史的原发性高血压以及女性高血压病密切相关.     

The coefficient of variation of RR intervals (CVRR) on electrocardiogram in patients with essential hypertension with reference to aging, hemodynamics and sympatho-adrenomedullary function]

To evaluate the significance of parasympathetic nerve activity in essential hypertension, we measured the coefficients of variation of RR intervals (CVRR) on electrocardiogram and examined the relationships between CVRR and aging, hemodynamics and sympatho-adrenomedullary function in normotensive subjects (NT) and in patients with essential hypertension (EHT). Mean arterial pressure (MAP), heart rate (HR), plasma noradrenaline concentration (pNA), plasma adrenaline concentration (pAd) and CVRR resting in a supine position were simultaneously measured in 37 NT (33.8 +/- 2.0 years) and 47 mild-to-moderate EHT (51.3 +/- 1.5 years). In both NT and EHT, significantly negative correlations between CVRR and age (NT: r = -0.54, p less than 0.001, EHT: r = -0.41, p less than 0.005) were observed, however, CVRR correlated with neither MAP, HR nor pAd. CVRR tended to correlate negatively with pNA (r = -0.27, p less than 0.1) in NT, unlike in EHT. The mean value of CVRR in EHT (n = 10, age: 38.3 +/- 1.6 years, CVRR: 3.61 +/- 0.37%) was significantly (p less than 0.005) lower than in age-matched NT (n = 10, age: 38.3 +/- 2.5 years, CVRR: 5.76 +/- 0.45%). These results indicate that the parasympathetic tone suggested by CVRR may be related to aging and sympathetic nerve activity, and that parasympathetic function might be impaired in EHT.     

肾性高血压患者的动态血压昼夜节律

本研究应用２４小时无创性全自动动态血压记录仪观察了６７例受试对象，其中肾实质性高血压（ＲＰＨＴ）１２例；肾血管性高血压（ＲｖＨＴ）Ⅱ例；Ⅰ～Ⅱ期原发性高血压（ＥＨＴ）４４例。结果表明，各组受试者的偶测血压均明显高于动态血压。ＲＰＨＴ和ＲＶＨＴ的昼夜节律均明显减弱，收缩压和舒张压的夜间下降值均明显小于原发性高血压患者，夜间下降率低于１０％者的比率却明显高于原发性高血压患者．ＥＨＴ的动态血压呈夜间下降、白昼上升的节律性。     

胰岛素抵抗--遗传和环境因素致高血压的共同途径?

目的　探讨胰岛素抵抗是否是遗传和环境因素致高血压的共同途径。方法　大庆地区具有血缘关系的三代内直系亲属 2 86核心家庭成员 858人 ,年龄 1 8～ 74岁。测血压、空腹血糖 (FPG)、胰岛素 (FINS)、胆固醇、甘油三酯、高密度脂蛋白胆固醇 (HDL C)、纤维蛋白原。计算胰岛素敏感性(ISI) =1 / (FPG×FINS) ,胰岛素抵抗 (IR) =(FPG×FINS) / 2 2 .5。以多因素回归分析探讨遗传和环境因素对血压水平的贡献。结果　原发性高血压组无论其有无阳性高血压家族史 ,胰岛素敏感性都较差。多因素逐步回归分析结果显示 ,胰岛素敏感性是高血压伴高血压家族史者、高血压不伴高血压家族史者及正常血压不伴高血压家族史 (且其配偶血压也正常 )者血压升高最重要的因素 ,能解释平均血压 (MBP)变化的 1 7% ;而空腹血糖、总胆固醇与HDL C 3项只能解释MBP变化的 9%。在分析自变量中加入高血压家族史一项时 ,则阳性高血压家族史成了血压升高最重要的因素 ,仅此一项就可解释MBP变化的 30 % ,而胰岛素敏感性对血压水平的贡献大幅度削弱 ,仅能解释MBP的 7%。对配偶组的分析显示同样趋势。结论　胰岛素抵抗是遗传及环境因素致高血压重要的共同途径 ,遗传因素还通过胰岛素抵抗以外的途径使血压升高     

Non-invasive assessment of microvascular endothelial function by laser Doppler flowmetry in patients with essential hypertension

The aim of the study was to investigate the endothelium-dependent vasodilation in the forearm skin using two non-invasive laser Doppler applications in patients with essential hypertension (EHT) and in normotensive (NT) control subjects. The effect of two consecutive doses of acetylcholine (ACh) and that of sodium nitroprusside (SNP) on the skin microcirculation, and thereafter the postocclusive reactive hyperaemic (PORH) response, were measured in 25 patients with essential hypertension and also in 25 control normotensive healthy subjects. The plasma von Willebrand factor (vWF) level and activity were also determined. The average peakflow in PORH was 287 +/- 31.5% (x +/- S.E.M.) in EHT and 410.28 +/- 35.08% in NT (P < 0.01). The average hyperaemic response to the two doses of ACh-iontophoresis was 206.36 +/- 33.97 and 568.76 +/- 54.23% in EHT and 444.24 +/- 80.28 and 804.12 +/- 93.07% in NT (P < 0.01, 0.05). The response to SNP was similar in the two groups. The vWF levels were 122.5 +/- 13.2 and 89.6 +/- 8.1% (P = 0.0595, NS), the activities were 80.8 +/- 5.5 and 68.9 +/- 6.1% (P = 0.157, NS) in EHT and in NT, respectively. These results demonstrate that essential hypertension is associated with endothelial dysfunction in the skin microcirculation of the forearm.     

A common mutation of low-density lipoprotein receptor gene is associated with essential hypertension among Japanese

Candidate genes offer one approach to the identification of the genetic susceptibility to hypertension. A common gene variant of the low-density lipoprotein (LDL) receptor gene (LDLR) that affects plasma LDL metabolism within the normolipidaemic range, may be such a candidate gene. A common mutation of LDLR, C1773T, was associated with lipid metabolism such that the T1773 allele increased plasma LDL levels in a Caucasian population. The present study examined whether C1773T/LDLR was associated with essential hypertension in a Japanese population. Subjects with essential hypertension (EHT, n = 300) with a family history of hypertension, and controls (NT, n = 310, sex- and age-matched with EHT) were recruited from among out-patients at Osaka University Hospital. A C1773T substitution at codon 570 in LDLR was determined using PCR-Hinc II-RFLP. It was revealed that the C1773 allele was significantly more frequent (0.89) among hypertensive patients (chi2 = 9.58, P < 0.01) than normotensives (0.83), the calculated odds ratio being 1.7 (95% CI: 1.2-2.4). The effect of the T1773 allele on increasing cholesterol was significant in normotensives without antihyperlipidaemic medication, but not in hypertensives. After adjustments of confounding factors, the estimated odds ratio for hypertension in the subjects with C1773 homozygote increased to 2.1 (95% CI: 1.3-3.5), suggesting that this polymorphism is an independent risk factor for hypertension. Our results show that the C1773 mutant of LDLR increases susceptibility to hypertension, but not via hypercholesterolaemia.     

Baroreflex sensitivity and heredity in essential hypertension.

BACKGROUND. Abnormalities in baroreflex control of heart rate may be important in the pathogenesis of essential hypertension. METHODS AND RESULTS. To investigate the influence of heredity on baroreflex function, we measured baroreflex sensitivity in 40 untreated patients with essential hypertension grouped by the presence (FH+) or absence (FH-) of a family history of hypertension and in 24 normotensive counterparts. Baroreflex sensitivity was assessed by both high-pressure (phenylephrine bolus) and low-pressure (amyl nitrite inhalation) stimuli. Subject groups were matched for age, blood pressure, body weight, and race. Baroreflex sensitivity (in milliseconds per millimeter of mercury) assessed by amyl nitrite inhalation was 24.3 +/- 2.8 in FH- normotensives, 12.3 +/- 1.7 in FH+ normotensives, 15.4 +/- 3.3 in FH- hypertensives, and 8.1 +/- 1.2 in FH+ hypertensives. Baroreflex sensitivity assessed by phenylephrine bolus was 28.8 +/- 5.6 in FH- normotensives, 19.3 +/- 2.8 in FH+ normotensives, 19.1 +/- 2.0 in FH- hypertensives, and 13.6 +/- 1.3 in FH+ hypertensives. Two-factor analysis of variance showed significant effects on baroreflex sensitivity for blood pressure status (normotensive versus hypertensive) and for family history of hypertension. After control line (controlling) for the effects of several variables, including age, mean arterial pressure, body weight, and race through multiple linear regression analysis, the effect of family history of hypertension on baroreflex sensitivity was still highly significant. Indeed, of all variables investigated, family history of hypertension was the strongest unique baroreflex sensitivity predictor. CONCLUSIONS. These data suggest that the impairment in baroreflex sensitivity in hypertension is in part genetically determined and may be an important hereditary component in the pathogenesis of essential hypertension.     

Higher urinary albumin excretion is associated with abnormal erythrocyte Na(+)/Li(+) countertransport (SLC) in non-modulating essential hypertensives and offspring of hypertensive parents

Non-modulating is a highly reproducible type of sodium-sensitive hypertension. The aim of this study was to evaluate in non-modulating individuals the erythrocyte sodium-lithium countertransport (SLC) abnormalities, which have been mentioned as a marker of non-modulation, and the association with increased microalbuminuria, as a marker of an early kidney impairment. We measured erythrocyte SLC in 10 normotensives (NT, 28 +/- 4 years), 20 offspring of hypertensive parents being 10 modulating (MHO, 25 +/- 6 years) and 10 non-modulating (NMHO, 26 +/- 5 years), and 23 essential hypertensives being 12 modulating (MHT, 34 +/- 5 years) and 11 non-modulating (NMHT, 32 +/- 4 years). In all the subjects studied, microalbuminuria was determined by duplicate 24-h urine collection by radioimmunoassay. In non-modulating offspring of hypertensive parents and essential hypertensives. SLC was significantly elevated when compared either with normotensives without family history of hypertension, modulating offspring of hypertensive parents or essential hypertensives (P < 0.025). Likewise, 24-h urinary albumin excretion was found higher in non-modulating individuals (essential hypertensives and offspring of hypertensive parents) than in modulating individuals (P < 0.01). In conclusion, non-modulators with higher SLC countertransport sodium transport abnormalities showed higher elimination of microalbuminuria suggesting that non-modulators may have an increased risk for developing cardiovascular morbidity and kidney impairment even in normotensive subjects with familiarity history of hypertension.     

Sympathetic neural mechanisms in white-coat hypertension

OBJECTIVES: This study planned to establish whether sympathetic hyperactivity exists in white-coat hypertension (WHT) in the clinical setting, relative to matched groups with normotension (NT) and untreated essential hypertension (EHT). BACKGROUND: White-coat hypertension differs from EHT by the presence of normal ambulatory blood pressure. Sympathetic hyperactivity exists in patients with EHT in the clinical setting and is believed to contribute to the development of target organ damage. Similar organ damage has been reported in WHT, yet little is known about sympathetic neural activity in this condition. METHODS: Using microneurography, we examined groups of 12 matched subjects with WHT, EHT and NT during the same clinical setting to quantify muscle sympathetic nerve activity as multiunit discharge (MSNA) and single units (s-MSNA). RESULTS: The s-MSNA in WHT (54 +/- 4.2 impulses/100 beats) was greater (p < 0.05) than in NT (37 +/- 5.4 impulses/100 beats) despite similar age and body mass index (BMI). The EHT values of s-MSNA (73 +/- 5.2 impulses/100 beats) were significantly (p < 0.05) greater than in WHT despite similar age, BMI and blood pressure levels. The MSNA followed a similar trend. White-coat hypertension had a similar cardiac baroreceptor reflex sensitivity to NT, but this was impaired in EHT relative to both NT and WHT. CONCLUSIONS: It was shown, in the clinical setting, that central sympathetic hyperactivity exists in WHT, albeit to a lesser degree than EHT. These findings suggest that WHT may not be entirely benign and that the observed sympathetic hyperactivity may be responsible for development of target organ damage in this group of patients.     

白大衣高血压患者的血小板功能

目的:探讨白大衣高血压(WCH)患者的血小板功能.方法:选初诊的原发性高血压(EH)患者、 WCH 患者、正常血压(NT)者各35例,通过诊室血压测量和24 h动态血压监测,同时测定并比较3组血小板最大聚集率(PAGTmax)、血浆血小板α-颗粒膜蛋白(GMP-140)含量、平均血小板容积(MPV) 、血小板数量的变化.结果:和NT对照组相比,EH组和WCH组 PAGTmax、血浆血小板GMP-140含量、MPV均明显增加(P<0.05)而三组血小板计数无统计学差异,同时EH组的PAGTmax、血浆血小板GMP-140含量、MPV均高于WCH组(P<0.05).EH组和WCH组MPV与24 h平均舒张压、GMP-140含量均正相关( P<0.05).结论:WCH存在血小板活化,可能和心血管事件发生率增加有关.     

The role of Na,K-ATPase inhibitor on pressor responsiveness in patients with benign essential hypertension

To clarify the role of Na,K-ATPase inhibitor in the enhanced pressor response to infused noradrenaline (NA-R) in patients with benign essential hypertension (EHT), NA-R, plasma noradrenaline concentration (PNA), and blood ionized calcium (Ca2+) were investigated before and after intravenous injection of ouabain in 15 normotensive subjects (NT) and 13 EHT. NA-R was enhanced by ouabain in both NT and EHT. The augmentation of NA-R following ouabain injection (delta NA-R) and % delta NA-R were significantly lower in EHT than in NT. Following ouabain injection, no significant change in PNA and blood Ca2+ was observed in both NT and EHT. NA-R negatively correlated with PNA and blood Ca2+, which were estimated just prior to noradrenaline infusion, before ouabain injection as well as after. After ouabain, the regression line between NA-R and PNA or blood Ca2+ shifted toward higher NA-R level in NT, unlike in EHT. These results suggest that an exogenous Na,K-ATPase inhibitor brings about a blunted enhancement of NA-R in EHT consistent with the presence of an endogenous Na,K-ATPase inhibitor in EHT.