Lack of association of the angiotensin converting enzyme gene polymorphism with essential hypertension in a chinese population

To examine the association between insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene and essential hypertension in a Chinese population, a case-control study was conducted using 157 hypertensive and 115 normotensive subjects. The I/D polymorphism of the ACE gene was identified by polymerase chain reaction. Plasma ACE activity was determined using spectrophotometry. The difference of allele frequencies between normotensives and hypertensives was statistically significant (X² = 4.467, P = .035), while the gentotype distribution was not different between normotensive and hypertensive subjects (X² = 3.954, P = .138). Plasma ACE activity was highest in the DD genotype, followed by the ID genotype, and the lowest in the II genotype (P = .0001 in normotensives and P = .163 in hypertensives, respectively). Thus, we conclude that the ACE gene polymorphism is not associated with essential hypertension in this Chinese population, but plasma ACE activity is genetically determined in the normotensive Chinese.     

Distribution of different HLA antigens in Greek hypertensives according to the angiotensin-converting enzyme genotype

The angiotensin-converting enzyme (ACE) insertion/deletion polymorphism is an independent risk factor for cardiovascular disease. It has also been suggested that some HLA genes may contribute to the genetic susceptibility to essential hypertension. So far, an association between ACE polymorphism and HLA antigens in arterial hypertension has not been reported. We have studied 94 subjects with newly diagnosed essential hypertension, 49 men and 45 women (mean age, 52.3 ± 11.3 years), as well as 104 randomly selected, age- and gender-matched normotensive individuals (54 men and 50 women, mean age 48.7 ± 10.8 years). Both cohorts originated from the Greek population and lived in the greater Athens area. The ACE genotype was analyzed by polymerase chain reaction. HLA class I and II antigens were studied by serologic and molecular techniques.The prevalence of the ACE genotypes did not differ significantly between hypertensives and normal individuals. The casual blood pressure levels and the average ambulatory blood pressure levels were similar among the three ACE genotypes. Hypertensives with the ACE-DD genotype were characterized by an increased prevalence of the HLA-A2 antigen (50% v 31.4%, P < .005) and DR6 (16.7% v 11.4%, P < .01) in comparison to the normotensive subjects with the ACE-DD genotype. HLA-A24 was found more frequently among the hypertensives with the ACE-ID genotype than in the normal controls with the same genotype (35.5% v 26.4%, P < .05). ACE-DD genotype is associated with a high prevalence of specific HLA antigens. The coexistence of the ACE-DD genotype with certain HLA phenotypes could reveal a distinct hypertensive population with increased risk for cardiovascular events.     

Angiotensin II stimulates left ventricular hypertrophy in hypertensive patients independently of blood pressure

Angiotensin II (AII) is known to be a growth stimulating factor for myocardial cells. We examined whether an exaggerated responsiveness to AII might aggravate left ventricular (LV) hypertrophy in human essential hypertension. To determine the responsiveness to AII in humans, we examined changes in mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR) (steady state input clearance technique with para-aminohippurate and inulin, respectively) and aldosterone secretion to AII infusions (0.5 and 3.0 ng/kg/min) in 71 normotensive male and 48 hypertensive male subjects (age: 26 ± 3 years; 24-h ambulatory blood pressure: 121 ± 5/71 ± 4 mmHg v 138 ± 7/82 ± 7 mmHg, P < .001). In addition, each patient underwent two-dimensional guided M-mode echocardiography at rest to assess cardiac structure and function. When given AII 3.0, a greater increase of MAP (13 ± 7 v 17 ± 8 mm Hg, P < .022) and a more marked decrease of RBF (−203 ± 123 mL/min v −270 ± 137 mL/min, P < .007) were found in hypertensives than in normotensives, whereas changes in GFR and aldosterone concentration were similar in both groups. Most important, changes in GFR to AII correlated with echocardiographically determined LV mass (normotensives: AII 0.5: r = 0.33, P < .006, AII 3.0: r = 0.28, P < .05; hypertensives: AII 0.5: r = 0.41, P < .006, AII 3.0: r = 0.32, P < .05). After taking baseline MAP and body mass index into account, the increase in GFR to AII 0.5 in hypertensives still correlated with LV mass (partial r = 0.37, P < .01). Inasmuch as the increase of GFR is a marker of the responsiveness to AII (related to vasoconstriction at the postglomerular site), our data suggest that increased sensitivity to AII is linked to LV hypertrophy in early essential hypertension, independently of the level of blood pressure.     

Hypertension and arterial stiffness: the atherosclerosis risk in communities study

Our objective was to describe the relationship of arterial stiffness and hypertension in a large, population-based sample of men and women. Hypertension-related increases in arterial stiffness may reflect the distending pressure and/or structural alterations in the artery. Included were 10,712 participants, ages 45 to 64 years, of the Atherosclerosis Risk in Communities Study, free of prevalent cardiovascular disease. Hypertension was classified as systolic or diastolic blood pressure (BP) ≥140/90 mm Hg, respectively, or the current use of antihypertensive medications. Common carotid arterial diameter change was measured using B-mode ultrasound and an electronic device that utilized radio frequency signals to track the motion of the arterial walls.Using statistical models to control for diastolic BP and pulse pressure, arterial diameter change was calculated separately in normotensive/nonmedicated and medicated hypertensives. Hypertension was associated with a smaller adjusted diameter change (ie, greater stiffness) in comparison to optimal blood pressure (BP < 120/80 mm Hg): normotensive/nonmedicated men, 0.33 versus 0.43 mm (P < 0.001); medicated men, 0.34 versus 0.42 mm (P < 0.001); normotensive/ nonmedicated women, 0.34 versus 0.40 mm (P < 0.001), and medicated women, 0.33 versus 0.40 mm (P < 0.001). The relationship between pulse pressure and diameter change (ie, the slope of pulse pressure and diameter change) did not differ between hypertensives and normotensives.These cross-sectional data suggest that hypertension is associated with carotid arterial stiffness; however, these differences in the calculated stiffness appear to be the effect of distending pressure rather than structural changes in the carotid artery.     

Relationship Between the Response to the Angiotensin Converting Enzyme Inhibitor Imidapril and the Angiotensin Converting Enzyme Genotype

Insertion (I)/deletion (D) polymorphism of the angiotensin converting enzyme (ACE) gene has been reported to be involved in various cardiovascular diseases. We investigated prospectively whether the response to the ACE inhibitor imidapril varied according to the ACE genotype or plasma ACE activity in Japanese hypertensive patients. The study population consisted of 57 hypertensive patients. After a 4-week observation period, imidapril was administered at a dose of 5 mg/day and blood pressure was measured every 2 weeks for 6 weeks. The plasma ACE activity in patients with the DD or ID genotype was significantly higher than that in patients with the II genotype. Neither the reduction nor the percent reduction in systolic blood pressure was significantly different between patients with either the DD or ID genotype and patients with the II genotype (DD or ID v II, 18.8 ± 2.4 v 20.2 ± 3.3 mm Hg; P = NS, 10.9 ± 1.4 v 11.7 ± 1.9%; P = NS, respectively). However, both the reduction and the percent reduction in diastolic blood pressure tended to be higher in patients with the II genotype (DD or ID v II, 7.9 ± 1.2 v 12.4 ± 2.2 mm Hg; P = .0669, 8.1 ± 1.2 v 12.4 ± 2.2%; P = .0569, respectively). The reduction in diastolic blood pressure was inversely correlated with plasma ACE activity (r = 0.301, P = .0253). In conclusion, the response to imidapril in hypertensive patients is determined at least in part by the ACE genotype.     

Angiotensin I Converting Enzyme Gene Polymorphism in Chinese Patients With Hypertension

Reports from different ethnic populations failed to show consistent findings on the association of hypertension with insertion/deletion (I/D) polymorphism of the angiotensin I converting enzyme (ACE) gene. In this population association study in Chinese, we compared the distribution of the ACE genotypes and allele frequency in 150 healthy controls with normal blood pressure and 148 hypertensive patients categorized by age. Although the frequencies of homozygote deletion (DD) genotype and deletion allele were greater in Chinese with hypertension than in normotensive controls (0.23 vs 0.13 and 0.44 v 0.37, respectively), the differences were not significant by χ² analysis (P = .07 and .09, respectively). Furthermore, we did not find the trend of decreasing number of DD genotype in older hypertensive Chinese patients. The results indicated a much lower prevalence of ACE/DD genotype in Chinese than in Caucasians and a modest association between I/D polymorphism of the ACE gene and hypertension in Chinese.     

Neutral endopeptidase and angiotensin I converting enzyme insertion/deletion gene polymorphism in humans

Neutral endopeptidase (NEP) hydrolyses angiotensins (Ang) I and II and generates angiotensin-(1-7) [Ang-(1-7)]. In humans, the insertion/deletion (I/D) angiotensin-I converting enzyme (ACE) gene polymorphism determined plasma ACE levels by 40%. In rats, a similar polymorphism determines ACE levels which are inversely associated to NEP activity. The objective of this study is to evaluate the relationship between ACE expression and plasma NEP activity in normotensive subjects and in hypertensive patients. In total, 58 consecutive patients with hypertension, evaluated in our Hypertension Clinic, were compared according to their ACE I/D genotypes with 54 control subjects in terms of both plasma ACE activity and NEP activities. Plasma ACE activity was elevated 51 and 70% in both DD ACE groups (normotensives and hypertensives) compared with their respective ID and II ACE groups (P<0.001). A significant effect of the ACE polymorphism and of the hypertensive status on ACE activity was observed (P<0.001). In normotensive DD ACE subjects, NEP activity was 0.30+/-0.02 U/ml, whereas in the normotensive II ACE and in the normotensive ID ACE subjects NEP activity was increased 65 and 48%, respectively (P<0.001). In the hypertensive DD ACE patients, NEP activity was 0.47+/-0.03 U/mg. An effect of the I/D ACE genotypes on NEP activity (P<0.04) and an interaction effect between the I/D ACE genotype and the hypertensive status were also observed (P<0.001). These results are consistent with a normal and inverse relationship between the ACE polymorphism and NEP activity in normotensive humans (as is also observed in rats). This normal relationship is not observed in hypertensive patients.     

Effect of l-arginine infusion on systemic and renal hemodynamics in hypertensive patients

This study was designed to compare the renal endothelial function in patients with essential hypertension and normal renal function with that in hypertensive patients with renal insufficiency. We studied the effects of l-arginine (500 mg/kg intravenously over 30 min) on renal hemodynamics in 30 normotensive control subjects, 32 patients with mild to moderate essential hypertension who had normal renal function, and seven hypertensive patients with renal insufficiency who had a serum creatinine concentration >2.0 mg/mL and a glomerular filtration rate <50 mL/min/1.48 m². l-Arginine infusion similarly reduced the mean blood pressure between the three groups (normotensive: −9.7% ± 0.7%, hypertensives with normal renal function: −10.2% ± 0.8%, and hypertensives with renal insufficiency: −8.2% ± 1.3%). The l-arginine–induced decrease in renal vascular resistance was smaller in essential hypertensive patients than in normotensive subjects (−11.0% ± 2.2 v −19.8% ± 2.1%, P <.05). However, l-arginine had no effect on the renal vascular resistance in hypertensive patients with renal insufficiency (1.6% ± 4.8%). Urine nitrite/nitrate levels in response to l-arginine significantly increased in the three groups in the following order: patients with renal insufficiency (47% ± 15%), essential hypertensive patients (87% ± 10%), and normotensive subjects (129% ± 12%). The glomerular filtration rate was unaffected by l-arginine in normotensive and essential hypertensive patients (3.1% ± 2.4% and 4.2% ± 2.5%), but significantly decreased in hypertensive patients with renal insufficiency (−13.7% ± 6.1%). These findings suggest that the ability of the l-arginine–nitric oxide–cGMP pathway to relax the renal vascular tone may be impaired in essential hypertensive patients and more markedly blunted in hypertensive patients with renal insufficiency, in parallel with increasing serum creatinine concentrations.     

White-coat hypertension and sex

OBJECTIVES: To compare, by sex, selected behavioral and biologic characteristics among normotensive, white-coat hypertensive, and essential hypertensive patients, and to assess the similarities and differences in these characteristics between men and women diagnosed as having white-coat hypertension. METHODS: The subjects of this study were 764 men (80 normotensives, 112 white-coat hypertensives, and 572 essential hypertensives) and 442 women (53 normotensives, 81 white-coat hypertensives and 308 essential hypertensives) who were a nonrandom subset of a larger cohort of patients being assessed to determine the prognostic significance of ambulatory blood pressure measurements. Physician-measured technician-measured and ambulatory (average awake and asleep) blood pressures, daytime blood pressure variability, the difference between awake and sleeping blood pressures, cholesterol levels, plasma renin activity (PRA) and anthropometric and demographic characteristics were compared across the patient classifications within each sex group and between male and female white-coat hypertensives using one-way analysis of variance. Student's t tests and chi squared analysis. RESULTS: Among men, cholesterol levels of normotensives were significantly lower than those of either white-coat or essential hypertensives (P < 0.05 and P < 0.01, respectively). White-coat hypertensives were significantly younger than the essential hypertensives. The ambulatory and technician-measured blood pressures of the white-coat hypertensives were similar to those of the normotensives, as were most measures of variability of blood pressure. Among women, there were no differences in cholesterol level; however, white-coat hypertensives had lower PRA than did the essential hypertensives (P < 0.01) In contrast to the men, women with white-coat hypertension were similar in age to those with essential hypertension, and 10 years older than normotensives (P < 0.01). The ambulatory blood pressures of white-coat hypertensives were similar to those of normotensives, but their technician-measured blood pressures were intermediate between those of the normotensive and essential hypertensive groups. The daily variability of diastolic blood pressure among the white-coat-hypertensive women was greater than that of the normotensive women and similar to that of the essential hypertensive women. For all other measures of variability, data for white-coat-hypertensive women were similar to those for the normotensive women. There was no anthropometric or demographic difference among the patients either for men or for women. White-coat-hypertensive women were older than white-coat-hypertensive men and had higher systolic blood pressures and variabilities of blood pressure (P < 0.05). They also had lower PRA. CONCLUSIONS: These results are consistent with the ideas that the phenomenon of white-coat hypertension is similar for the two sexes, women may exhibit white-coat hypertension at a greater age than do men, and women with white-coat hypertension may further exhibit a broader white-coat effect, reflected in blood pressures measured by other medical personnel.     

Prevalence of left ventricular hypertrophy in a hypertensive population

AIMS: This investigation was set up to study the prevalence of leftventricular hypertrophy in a hypertensive population with referenceto a normotensive control group. From the general population3498 men and women aged 35, 45, 55 and 65 years old were invitedto a health examination. Participants with blood pressure above160 mmHg systolic or 95 mmHg diastolic or those taking antihypertensivemedication or having done so during the previous 6 months wereasked to undergo an echocardiographic examination. Normotensivecontrols were randomly selected from the same population. Of552 participants in the final study population, 194 were normotensivecontrols and 358 were in the hypertensive group. Echocardiographicmeasurements were made according to the Penn conventions andindexed for body surface. Cut-off values for left ventricularhypertrophy were 134 g. m^{– 2} for males and 102 g. m^–2 for women. RESULTS: Overall, the prevalence of left ventricular hypertrophy wasl4%/20% (men/women) in normotensives and 25%/26% in hypertensives(P<0·01). After subdivision by age and sex, therewas a significant difference in the prevalence of left ventricularhypertrophy between normotensives and hypertensives only inthe 65-year-old group (P<0·02 for males and P<0·05for females). CONCLUSION: The association between blood pressure and left ventricularhypertrophy in the general population is weak. Left ventricularhypertrophy is only significantly more frequent among hypertensivesas compared to normotensives in older people.     

不同性别血管紧张素转化酶基因型与原发性高血压相关性研究

目的 :探讨男、女不同性别的血管紧张素转化酶 (ACE)基因型与原发性高血压 (EH)的相关关系。方法 :应用聚合酶链反应 (PCR)技术检测 12 8例男性 (其中EH患者 73例 ) ,79例女性(其中EH患者 4 3例 )ACE基因插入 /缺失 (I/D)多态性。结果 :男性组EH患者DD基因型频率(0 .35 6 )和D等位基因频率 (0 .5 75 )显著高于对照者 (0 .182和 0 .4 2 7,分别P <0 .0 5 ,<0 .0 2 )。且ACEDD基因型与男性EH患者的收缩压和脉压增高有关 (P <0 .0 5 )。而女性ACE基因型与EH及血压无显著相关性存在 (均P >0 .0 5 )。结论 :ACE基因I/D多态性对男性EH的发生及血压的增高有显著影响 ,而对女性无此作用。     

Angiotensin-converting enzyme gene I/D polymorphism increases the susceptibility to hypertension and additive diseases: A study on North Indian patients

Angiotensin-converting enzyme (ACE) is the key enzyme of the renin angiotensin system (RAS) which maintains the blood pressure homeostasis in our body. The association of the ACE insertion/deletion (I/D) polymorphism with essential hypertension has been demonstrated by many studies. The purpose of the present study is to investigate the association of the insertion/deletion polymorphism of the ACE gene with hypertension and additive diseases in North Indian population. In total, 222 hypertensive and 218 normotensive adults participated in this hospital-based study. Anthropometric measures, lipids profiles, blood glucose, and blood pressure (BP) measures were collected from participants. ACE I/D polymorphism was determined by using insertion-specific amplification. The mean ages of study groups were 50.35 ± 12.40 and 47.32 ± 11.94 for cases and controls, respectively. Significant differences were observed in the frequencies of DD, ID, and II genotypes among the hypertensive and normotensive groups which were found to be 29.7%, 38.7%, and 31.5% vs. 53.7%, 23.4%, and 22.9%, respectively. It has been observed that the ACE ID genotype was significantly (p < 0.05) higher in hypertensive subjects, whereas, the DD genotype was significantly (p < 0.05) higher in control subjects. A strong association was found between cardiovascular diseases (CVDs) and ID genotype [p = 0.017, odds ratio (OR) = 3.091, 95% confidence interval (CI) = 1.224–7.807]. ID [p = 0.002, OR = 2.020, 95% CI = 1.281–3.185] and II [p = 0.032, OR = 1.677, 95% CI = 1.044–2.694] genotypes are more prone to diabetes with hypertension. This finding suggests that ACE insertion/deletion polymorphism is associated with hypertension and additive diseases in North Indians.     

Carotid thickening,cardiac hypertrophy,and angiotensin converting enzyme gene polymorphism in patients with hypertension

An insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene has been associated with increased risk for myocardial infarction, cardiomyopathy, carotid thickening, and cardiac hypertrophy. However, a conclusive agreement about the role of ACE genotype in the genetics of cardiovascular disease has not yet been reached. This study was undertaken to investigate the relationship of the I/D polymorphism of the ACE gene with carotid intima-media thickness (IMT) and left ventricular mass (LVM) in 175 Chinese patients with mild-to-moderate hypertension. The I/D genotypes were detected by the polymerase chain reaction using primers flanking the polymorphic region in intron 16 of the ACE gene. The IMT was measured in the common carotid and carotid bifurcation by B-mode ultrasound. The LVM was calculated with M-mode echocardiographic measures of the left ventricle. Patients with the DD genotype (n = 41) showed significant greater carotid IMT (1.593 ± 0.879 v1.309 ± 0.703 and 1.171 ± 0.583 mm, P = .01) but insignificant higher LVM index (123.8 ± 36.6 v 123.7 ± 37.4 and 118.2 ± 33.0 g/m², P = .61) than did those with the DI (n = 69) and II (n = 65) genotypes. The deletion polymorphism of the ACE gene (P = .04) was a significant predictor for carotid IMT on multiple regression analysis, controlling all the potential confounding factors including age (P = .001), systolic blood pressure (P = .09), smoking (P = .08), and plasma tissue plasminogen activator antigen (P = .03), but the LVM correlated only with age (P = .02), sex (P < .001), and body mass index (P < .001). These results indicated that the DD genotype of the ACE gene could be considered a risk factor for the development of early atherosclerosis in carotid arteries but not for left ventricular hypertrophy in the hypertensive population.     

Urinary albumin excretion — A predictor of risk of cardiovascular disease: A prospective 10-year follow-up of middle-aged nondiabetic normal and hypertensive men

To study how the risk of cardiovascular disease changes with increasing levels of urinary albumin excretion (UAE), we prospectively studied a random sample of 120 49-year-old men with a wide range of blood pressures. Based on diastolic blood pressure (DBP), the subjects were divided into normotensives (DBP < 90 mm Hg; n = 21), borderline hypertensives (DBP 90 to 94 mm Hg; n = 30), mild hypertensives (DBP 95 to 104 mm Hg; n = 45) and moderate to severe hypertensives (DEP > 105 mm Hg; n = 24). None had been previously treated for hypertension or had secondary hypertension, diabetes mellitus, or other cardiovascular diseases at baseline. Heart and kidney function and metabolic and hormonal variables were also studied. The hypertensives were treated with β-blockade, diuretics, or hydralazine. The cardiovascular morbidity during 10 years of follow-up was studied.The 19 subjects who developed cardiovascular disease had significantly higher baseline UAE than the group that did not (median value 16.6 mg/24 h; range 3.5 to 73, and 9.7 mg/24 h, range 0 to 308, respectively). UAE correlated to systolic blood pressure (P = .0115) and DBP (P = .031), but not to smoking behavior or serum cholesterol. The risk of cardiovascular disease was associated with UAE and smoking independently of blood pressure (P = .001 and P = .015, respectively), and the risk increased continuously with increasing UAE.The initial UAE thus emerged as an efficient and independent predictor of cardiovascular disease in middle-aged hypertensive and normotensive men. UAE appeared to be a stronger predictor than blood pressure and serum cholesterol.     

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.     

Effects of α1-Blockade on the Forearm Vascular Resistance Responses to Lower Body Negative Pressure in Young Borderline Hypertensives

To determine whether α₁-blockade affects the forearm vascular resistance responses to lower body negative pressure (LBNP) in borderline hypertensives, six hypertensives (HTN; mean arterial pressure [MAP] = 109.9 ± 1.7 mm Hg, mean ± SE) and seven normotensives (NTN; MAP = 81.5 ± 1.4 mm Hg) underwent exposures of LBNP at pressures of −10, −20, and −40 mm Hg during systemic α₁-receptor blockade (BLK) and during placebo (PLA). Resting forearm vascular resistance (FVR) was greater in HTN than in NTN during PLA (34.8 ± 5.4 v 17.5 ± 3.1 units; P < .05), but not during BLK (28.1 ± 5.2 v 25.3 ± 9.9 units). When expressed as a percentage of resting FVR, LBNP evoked an increased FVR (P < .001) that did not differ significantly between BLK and PLA in either group. FVR was higher (P < .001) in HTN than in NTN throughout both trials; at −40 mm Hg of LBNP during BLK, the increase in FVR was greater (P < .05) in HTN than in NTN (131 ± 42 v 48 ± 15%). MAP (relative to resting) was maintained throughout LBNP during PLA but, at −40 mm Hg, was lower (P < .01) during BLK for both groups. HR was elevated in BLK and was increased at −40 mm Hg (P < .01) for each group in each trial. This increase was greater during BLK (P < .05). These data suggest that borderline hypertensives have a greater vasoconstrictor response to LBNP than do normotensives and α₁-blockade does not appear to attenuate this response.     

中国汉族人血管紧张素转换酶基因I/D多态性与原发性高血压的关系

目的探讨ＡＣＥ基因Ｉ／Ｄ多态性在中国汉族人群分布规律及与原发性高血压（ＥＨ）的关系。方法取汉族ＥＨ病人１２１例，对照组９５人外周血，提取ＤＮＡ，应用ＰＣＲ技术进行ＡＣＥ基因Ｉ／Ｄ分型。结果在汉族血压正常群体中，ＡＣＥ基因Ｉ／Ｄ多态ＤＤ、ＤＩ、Ｉ基因型频率分别为２２％，４８％和３０％，其Ｄ和Ｉ等位基因频率分别为４６％和５４％。Ｉ／Ｄ多态分布符合Ｈａｒｄｙ－Ｗｅｉｎｂｅｒｇ定律，达到遗传平衡，具有群体代表性。ＥＨ组与正常组相比，基因型和等位基因分布均具有显著统计学差异（Ｐ＜０．０５），ＥＨ组ＤＤ基因型和Ｄ等位基因频率增加。结论汉族ＥＨ发病与ＡＣＥ基因Ｉ／Ｄ多态性相关联，基因型ＤＤ和等位基因Ｄ可能是ＥＨ发病的易患因素     

Significance of the Measurement of Urinary Alanine Aminopeptidase and N-Acetyl-β-D-Glucosaminidase Activity in Evaluating Patients with Essential Hypertension

To examine the relationship between the urinary levels of alanine aminopeptidase (AAP) or N-acetyl-β-D-glucosaminidase (NAG) and the advance of essential hypertension, we measured the urinary levels of these enzymes in 20 normotensive controls, 8 subjects with borderline hypertension and 40 subjects with WHO stage I and stage II essential hypertension. The urinary level of NAG in stage II hypertensives was higher than that in the normotensives, and borderline or stage I hypertensives (p < 0.01). Systolic blood pressure and the urinary level of NAG was positively correlated in hypertensives (rs=0.43, p < 0.01). The urinary level of NAG was correlated inversely with renal blood flow (rs=-0.61, p < 0.01). The urinary level of AAP in stage II hypertensives was also higher than that in the normotensives (p < 0.01) or stage I hypertension (p < 0.01), but the urinary AAP level was not significantly correlated with systolic blood pressure or renal blood flow in hypertension.     

Associations between angiotensinogen gene variants and left ventricular mass and function in the HyperGEN study

Background The angiotensinogen M235T polymorphism is positively associated with plasma angiotensinogen, hypertension, and coronary heart disease. However, the association of M235T polymorphism with left ventricular (LV) mass and function is not well defined at the population level. We investigated whether 2 tightly linked polymorphisms of angiotensinogen gene, M235T and G-6A, are associated with LV mass and function in a large population-based sample, composed mostly of patients with hypertension. Methods Two-dimensional guided M-mode and pulsed Doppler scan echocardiograms were performed in 605 participants. The angiotensinogen M235T was analyzed with a standard polymerase chain reaction test, and the G-6A variant was measured with mass spectrophotometry. Results The association of angiotensinogen gene to LV mass and LV mass indexed to body surface area (LVMI) differed significantly between subjects with normotensive and hypertensive conditions with respect to the direction of association (P < .005). The methionine-threonine/threonine-threonine genotype was negatively associated with LV mass and LVMI in patients with hypertension after adjustment for blood pressure, antihypertensive medication use, weight, and other covariates (P < .001), and patients with normotensive conditions with the methionine-threonine/threonine-threonine genotype had higher LV mass and LVMI (P = .04, for LV mass; P = .14, for LVMI). The association in patients with normotensive conditions was not influenced by blood pressure but was partly confounded by weight. Conclusion Variation in the angiotensinogen gene was modestly associated with LV mass independently of covariates in patients with hypertensive conditions. The direction of the association was opposite to that observed in patients with normotensive conditions, probably because of the influence of other risk factors or antihypertensive medication use or both. (Am Heart J 2002;143:854-60.)