The environmental and genetic evidence for the association of hyperlipidemia and hypertension.

Abstract

Both hyperlipidemia and hypertension are the risk factors for coronary heart disease. Although studies have shown that there is an association between plasma lipid and blood pressure levels, the association of hyperlipidemia and hypertension is still not well established. The present study was undertaken to compare the differences in several environmental and genetic factors between hyperlipidemia and hypertension in the Guangxi Hei Yi Zhuang population.
A total of 1669 participants were surveyed by a stratified randomized cluster sampling. Information on environmental factors was collected with standardized questionnaires. Genotyping of angiotensin-converting enzyme, angiotensinogen, angiotensin receptor 2, apolipoprotein (apo) A-I, apoB, apoE, cholesteryl ester transfer protein, G-protein beta-3 subunit, hepatic lipase, lipoprotein lipase, microsomal triglyceride transfer protein, regulator of G-protein signaling 2, and sterol regulatory element-binding protein-2 was also performed.
There were 358 (21.45%) participants with isolated hyperlipidemia, 257 (15.40%) with isolated hypertension, 189 (11.32%) with both conditions, and 865 (51.83%) normals. Hyperlipidemia was positively correlated with age, BMI, alcohol consumption, total energy and total fat intake, apoE, and microsomal triglyceride transfer protein genotypes, and negatively associated with total dietary fiber intake, apoA-I, and lipoprotein lipase genotypes. Hypertension was positively correlated with male sex, age, hyperlipidemia, total energy, total fat, and sodium intake, apoE, angiotensin receptor 2, and microsomal triglyceride transfer protein genotypes, and negatively associated with education level, total dietary fiber intake, angiotensin-converting enzyme, apoA-I, and lipoprotein lipase genotypes.
These findings suggest that hyperlipidemia and hypertension have many common risk factors. Hyperlipidemia is associated with hypertension in many aspects.

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The environmental and genetic evidence for the association
of hyperlipidemia and hypertension
Yin Ruixinga, Wu Jinzhena, Lin Weixiongb, Chen Yuminga, Yang Dezhaiband
Pan Shanglingc
Objective Both hyperlipidemia and hypertension are the
risk factors for coronary heart disease. Although studies
have shown that there is an association between plasma
lipid and blood pressure levels, the association of
hyperlipidemia and hypertension is still not well
established. The present study was undertaken to compare
the differences in several environmental and genetic factors
between hyperlipidemia and hypertension in the Guangxi
Hei Yi Zhuang population.
Methods A total of 1669 participants were surveyed by a
stratified randomized cluster sampling. Information on
environmental factors was collected with standardized
questionnaires. Genotyping of angiotensin-converting
enzyme, angiotensinogen, angiotensin receptor 2,
apolipoprotein (apo) A-I, apoB, apoE, cholesteryl ester
transfer protein, G-protein b-3 subunit, hepatic lipase,
lipoprotein lipase, microsomal triglyceride transfer protein,
regulator of G-protein signaling 2, and sterol regulatory
element-binding protein-2 was also performed.
Results There were 358 (21.45%) participants with isolated
hyperlipidemia, 257 (15.40%) with isolated hypertension,
189 (11.32%) with both conditions, and 865 (51.83%)
normals. Hyperlipidemia was positively correlated with age,
BMI, alcohol consumption, total energy and total fat intake,
apoE, and microsomal triglyceride transfer protein
genotypes, and negatively associated with total dietary fiber
intake, apoA-I, and lipoprotein lipase genotypes.
Hypertension was positively correlated with male sex, age,
hyperlipidemia, total energy, total fat, and sodium intake,
apoE, angiotensin receptor 2, and microsomal triglyceride
transfer protein genotypes, and negatively associated with
education level, total dietary fiber intake, angiotensin-
converting enzyme, apoA-I, and lipoprotein lipase
genotypes.
Conclusion These findings suggest that hyperlipidemia
and hypertension have many common risk factors.
Hyperlipidemia is associated with hypertension in many
aspects. J Hypertens 27:251–258 Q 2009 Wolters Kluwer
Health | Lippincott Williams & Wilkins.
Journal of Hypertension 2009, 27:251–258
Keywords: blood pressure, genetic polymorphisms, hyperlipidemia,
hypertension, lipids, risk factors
Abbreviations: ACE, angiotensin-converting enzyme; AGT,
angiotensinogen; Apo, apolipoprotein; ATR2, angiotensin receptor 2;
CETP, cholesteryl ester transfer protein; GNB3, G-protein b-3 subunit;
HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein
cholesterol; LIPC, hepatic lipase gene; LPL, lipoprotein lipase; MTP,
microsomal triglyceride transfer protein; RGS2, regulator of G-protein
signaling 2; SREBP-2, sterol regulatory element-binding protein-2
aDepartment of Cardiology, Institute of Cardiovascular Diseases, the First
Affiliated Hospital,bDepartment of Molecular Biology, Medical Scientific
Research Center andcDepartment of Pathophysiology, School of Premedical
Sciences, Guangxi Medical University, Nanning, Guangxi, People’s Republic of
China
Correspondence to Professor Yin Ruixing, MD, Department of Cardiology,
Institute of Cardiovascular Diseases, the First Affiliated Hospital, Guangxi Medical
University, 22 Shuangyong Road, Nanning 530021, People’s Republic of China
Tel: +86 771 5358263; fax: +86 771 5353342;
e-mail: yinruixing@yahoo.com.cn
Received 19 June 2008 Revised 3 October 2008
Accepted 2 October 2008
Introduction
Both hyperlipidemia and hypertension are the com-
ponents of the metabolic syndrome [1] and are also
identified as independent risk factors for coronary heart
disease [2]. Blood pressure and plasma lipids have been
found to be consistently related in several populations
[3–11]. Some reports have observed a close link between
elevated blood pressure and dyslipidemia in hyperten-
sive patients [12,13]. A study from the USA has found
that approximately 12% of persons with high blood
pressure have a syndrome called ‘familial dyslipidemic
hypertension’. Elevated blood lipid levels of these
patients are two or three times as common as expected
[14]. Hyperlipidemia and hypertension are complex mul-
tifactorial and polygenic disorders that are thought to
resultfromaninteractionbetweenanindividual’sgenetic
background and various environmental factors. In recent
years, a number of studies such as genetic linkage
analyses and/or candidate gene association studies have
been performed to elucidate the contribution of genetic
factors to both conditions. Allayee et al. [15] found a locus
on chromosome 4 that was associated with a four-fold
increase in the likelihood of developing systolic high
blood pressure as well as with a concomitant increase
in plasma free fatty acid concentrations. Moreover, a
locus on chromosome 19p was detected in Dutch adults
Original article251
0263-6352 ? 2009 Wolters Kluwer Health | Lippincott Williams & WilkinsDOI:10.1097/HJH.0b013e32831bc74d

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that provided a link between systolic blood pressure and
high apolipoprotein (apo) B levels [15]. Sprecher et al.
[16] observed that 38 individuals heterozygous for lipo-
protein lipase (LPL) mutations not only had elevated
triglycerides and lower high-density lipoprotein choles-
terol (HDL-C) compared with 95 family members
without the LPL gene defect, but also had higher blood
pressure levels, suggesting that a LPL gene defect may
contribute to the expression of systolic blood pressure.
These genetic observations indicate that multiple
genetic factors exist that may affect both the blood
pressure and serum lipid levels. However, few studies
have shown the association of hyperlipidemia and hyper-
tension by the combined analysis of multiple environ-
mental and genetic factors. In addition, because of the
ethnic divergence of gene polymorphisms, it is important
to examine polymorphisms related to hyperlipidemia and
hypertension in each ethnic group.
Zhuang is the largest minority among 56 ethnic groups in
China. Geographically and linguistically, Zhuang can be
classified into 43 ethnic subgroups, in which Hei Yi
(means black worship and black dressing) Zhuang is
considered to be the most conservative subgroup. The
population size is 51655 individuals. Because of isolation
from the other ethnic group, the special customs and
cultures, including their black clothing, intra-ethnic
marriages, dietary habits,and lifestylearestillcompletely
conserved to the present day [17]. In a previous cross-
sectional study, we have shown that hyperlipidemia was
positively correlated with hypertension in this population
[17]. We hypothesize that there may be some common
environmental and genetic predisposing factors between
blood pressure regulation and lipid metabolism. There-
fore, the aim of the present study was to compare the
differences in several environmental and genetic factors
between hyperlipidemia and
Guangxi Hei Yi Zhuang population.
hypertensioninthe
Methods
Participants
A total of 1669 participants of Hei Yi Zhuang residing in
seven villages in Napo County, Guangxi Zhuang
Autonomous Region, China were surveyed by a stratified
randomized cluster sampling. The ages of the partici-
pants ranged from 15 to 84 years, with an average age of
46.05?15.30 years. All study participants were peasants.
The participants accounted for 3.23% of total Hei Yi
Zhuang population. In the analysis, the participants with
a history of chronic illness, including hepatic, renal,
thyroid, diabetes mellitus, myocardial infarction, stroke,
or congestive heart failure were rejected. Thirty partici-
pants were treated with antihypertensive drugs such as
nifedipine and/or catopril, but no one used lipid-lowering
drugs such as statins or fibrates, b-blockers, diuretics, or
hormones. The present study was approvedby the Ethics
Committee of the First Affiliated Hospital, Guangxi
Medical University. Informed consent was obtained from
all participants after they received a full explanation of
the study.
Epidemiological survey
The survey was carried out using internationally stan-
dardized methods [18], following a common protocol.
Information on demographics, socioeconomic status,
cigarette smoking, alcohol consumption, and physical
activity was collected with standardized questionnaires.
Current smoking was defined as more than one cigarette
per day. Participants who reported having smoked at
least 100 cigarettes during their lifetime were classified
as current smokers if they currently smoked and former
smokers if they did not. Consumption of alcohol included
questions about the number of grams of rice wine, wine,
beer, or liquor consumed during the preceding 12
months. The 24-h dietary recall method was used to
determine the dietary intake of each participant [19].
Detailed descriptions of all foods, beverages, and supple-
ments consumed during the 24-h period before the inter-
view, including the quantity, cooking method, and brand
names were recorded by a chief physician. The inter-
viewer used food models and pictures depicting portion
sizes and followed a standardized protocol for determin-
ing the weight of the food consumed. The intake of
macronutrients from the ingredients was determined by
using the 2002 Chinese Food Composition Table [20].
Overall physical activity was ascertained with the use of a
modified version of the Harvard Alumni Physical Activity
Questionnaire [21]. For the physical examination, height,
weight, waist circumference, and BMI (in kg/m2) were
calculated. Sitting blood pressure was measured three
timeswiththeuseofamercurysphygmomanometerafter
the participant rested for 5min, and the average of the
three measurements was used for the level of blood
pressure. Systolic blood pressure was determined by
the first Korotkoff sound and diastolic blood pressure
by the fifth Korotkoff sound. Waist circumference was
measured with a nonstretchable measuring tape, at the
level of the smallest area of the waist, to the nearest
0.1cm.
Measurements of lipids and apolipoproteins
Blood sample was drawn from an antecubital vein in all
participants after an overnight fast. The blood was trans-
ferred into glass tubes and allowed to clot at room
temperature. Immediately following clotting serum was
separated by centrifugation for 15min at 3000rpm. The
levels of total cholesterol, triglycerides, HDL-C, and
low-density lipoprotein cholesterol (LDL-C) in samples
were determined enzymatically using commercially
available kits (RANDOX Laboratories Ltd., Ardmore,
UK and Daiichi Pure Chemicals Co., Ltd., Tokyo,
Japan), respectively. Serum apoA-I and apoB levels were
measured by an immunoturbidimetric assay (RANDOX
Laboratories Ltd.). All determinations were performed
252
Journal of Hypertension
2009, Vol 27 No 2

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with an autoanalyzer (Type 7170A; Hitachi Ltd., Tokyo,
Japan) in the Clinical Science Experiment Center of the
First Affiliated Hospital, Guangxi Medical University
[22].
Genotyping
Genomic DNA was extracted from the peripheral blood
leukocytes by the phenol-chloroform method as shown in
our previous reports [23,24]. The extracted DNA was
stored at 48C until analysis. Genotyping of angiotensin-
converting enzyme (ACE), angiotensinogen (AGT),
angiotensin receptor 2 (ATR2), apoA-I, apoB, apoE,
cholesteryl ester transfer protein (CETP), G-protein
b-3 subunit (GNB3), hepatic lipase (LIPC), LPL,
microsomaltriglyceridetransferprotein(MTP),regulator
of G-protein signaling 2 (RGS2), and sterol regulatory
element-binding protein-2 (SREBP-2) was performed
using polymerase chain reaction and restriction fragment
length polymorphism or allele-specific oligonucleotides.
The thermocycling protocol, the approach to electropho-
resis, and the procedures for quality control have been
described previously [23,24].
Diagnostic criteria
Hypertension was defined as an average systolic pressure
of 140mmHg or greater and/or an average diastolic pres-
sure of 90mmHg or greater, and/or self-reported pharma-
cological treatment for hypertension within the 2 weeks
priortotheinterview[17,25].Thenormalvaluesofserum
total cholesterol, triglycerides, HDL-C, LDL-C, apoA-I,
apoB, and the ratio of apoA-I to apoB in our Clinical
Science Experiment Center were 3.10–5.17, 0.56–1.70,
0.91–1.81, 1.70–3.20mmol/l, 1.00–1.76, 0.63–1.14g/l,
and 1.00–2.50, respectively. The individuals with total
cholesterol more than 5.17mmol/l and/or triglycerides
more than 1.70mmol/l were defined as hyperlipidemic
[22–24]. Normal weight, overweight, and obesity were
defined as a BMI less than 24, 24–28, and more than
28kg/m2, respectively [26].
Statistical analysis
The data are presented as mean?SD or percentage. All
statistical analyses were performed using SAS 9.1. (SAS
Institute, Inc., Cary, North Carolina, USA). Chi square
testswereusedtocomparethedifferencesinpercentages
and to assess Hardy–Weinberg expectations, whereas
analysis of covariance (ANOVA) was used to compare
the differences in various continuous variables between
respective comparison groups. The factors such as sex,
age, education level, physical activity, BMI, waist
circumference, alcoholconsumption,
smoking were adjusted for the statistical analyses. In
order to evaluate the risk factors for hyperlipidemia
and hypertension, unconditional logistic regression
analysis was also performed in the population. The back-
ward multiple logistic regression method was used
to select the risk factors significantly associated with
andcigarette
hyperlipidemia or hypertension. P<0.05 was considered
statistically significant.
Results
General characteristics between hyperlipidemia and
hypertension
As shown in Table 1, there were 358 (21.45%) parti-
cipants with isolated hyperlipidemia, 257 (15.40%) with
isolated hypertension, 189 (11.32%) with both hyper-
lipidemia and hypertension, and 865 (51.83%) normals.
The average age, the ratio of men to women, the per-
centages of participants who consumed alcohol, and
protein and salt intake were higher in participants with
hypertension than those with hyperlipidemia (P<0.05–
0.01). On the contrary, the education level, the percen-
tages of participants with a BMI more than 24kg/m2,
waistcircumference,totalfatandtotaldietaryfiberintake
were lower in participants with hypertension than those
with hyperlipidemia. The levels of HDL-C, LDL-C,
apoA-I, and apoB were also lower in participants with
hypertension than those with hyperlipidemia (P<0.05–
0.01). There were no significant differences in the
weight, BMI, cigarette smoking, total energy and carbo-
hydrateintakebetweenhypertensiveandhyperlipidemic
patients (P>0.05 for all).
Genotypic frequencies between hyperlipidemia and
hypertension
The genotypic frequencies in participants with hyper-
lipidemia and hypertension are shown in Table 2. There
were significant differences in the genotypic frequencies
of apoA-I, apoE, LPL, and MTP between normal
group and the participants with isolated hyperlipidemia,
isolated hypertension, or both hyperlipidemia and hyper-
tension (P<0.05–0.001). However, there were no signi-
ficant differences in the genotypic frequencies of apoA-I,
apoE, LPL, and MTP among the participants with
isolated hyperlipidemia, isolated hypertension, or both
hyperlipidemia and hypertension (P>0.05). There were
also significant differences in the genotypic frequencies
of ACE and ATR2 between hypertensive and normal or
isolated hyperlipidemia group (P<0.05–0.001). No signi-
ficant difference in the genotypic frequencies of AGT,
apoB, CETP, GNB3, LIPC, RGS2, and SREBP-2 was
identified among the four groups (P>0.05).
Risk factors for hyperlipidemia and hypertension
The results of multivariate logistic regression analysis are
shown in Table 3. Hyperlipidemia was positively corre-
lated with age, BMI, alcohol consumption, total energy
and total fat intake, apoE, and MTP genotypes, and
negatively associated with total dietary fiber intake,
apoA-I, and LPL genotypes (P<0.05–0.001). Hyperten-
sion was positively correlated with male sex, age, hyper-
lipidemia, total energy, total fat, and sodium intake,
apoE,ATR2,andMTPgenotypes,and negativelyassoci-
ated with education level, total dietary fiber intake, ACE,
Association of hyperlipidemia and hypertension Ruixing et al.
253

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apoA-I, and LPL genotypes (P<0.05–0.001). There was
no significant association of either hyperlipidemia or
hypertension with physical activity, waist circumference,
cigarette smoking, dietary cholesterol, and AGT, apoB,
CETP, GNB3, LIPC, RGS2, or SREBP-2 genotypes
(P>0.05 for all).
Discussion
Environmental factors for the association of
hyperlipidemia and hypertension
Serum lipid metabolism and blood pressure regulation
have been associated in several cross-sectional studies
[3–5]. Blood pressure and serum total cholesterol levels
were strongly correlated among hypertensive patients,
which led to early recommendations to treat elevated
cholesterol in patients with hypertension [4,6]. In the
present study, we also show no significant differences
in the weight, BMI, cigarette smoking, total energy,
and carbohydrate intakes between hyperlipidemic and
hypertensive patients.
In our study, we found that the average age of the
participants was more in hypertension than in hyperlipi-
demia group. This finding suggests that previous hyper-
lipidemia may be one of the causes of future hyperten-
sion [2]. Several studies [7–9] have prospectively
examined the relationship between plasma lipids and
the future development of hypertension, revealing that
there is an association between plasma lipids and the
development of hypertension. Higher levels of plasma
total cholesterol, non-HDL-C, and the total cholesterol/
HDL-C ratio were independently associated with a sub-
sequent increased risk of incident hypertension in appar-
ently healthy men. Elevated lipid levels appeared to
predate the onset of hypertension by years [9–11]. In
the present study, we also show that hypertension was
positively correlated with hyperlipidemia. These results
suggest that hyperlipidemia is associated with hyperten-
sion. Dyslipidemia is known to influence endothelial
function through a number of different mechanisms
[27]. Endothelial dysfunction has been documented in
individuals with increased levels of remnant lipoproteins
[28], and endothelium-dependent vasodilation in res-
ponse to acetylcholine or shear stress has been shown
to be impaired in hypertriglyceridemic individuals
[29,30]. The loss of physiological vasomotor activity that
254
Journal of Hypertension
2009, Vol 27 No 2
Table 1
Comparison of general characteristics, blood pressure, and serum lipid levels among the four groups
Characteristics Normal (n¼865)Hyperlipidemia (n¼358)
47.05?15.68a
150/208
3.78?1.45a
36.56?12.04
152.84?8.69
50.28?8.10
21.44?2.39
59 (16.48)a
74.33?7.68a
188 (52.51)
105 (29.33)
8833?323a
295.25?22.23a
76.32?7.37a
62.64?6.93a
198.71?128.82c
8.88?3.16a
7.78?2.67
119.32?10.85a
73.99?8.58
45.44?10.70a
0
0
0
5.49?0.96a
289 (80.73)
1.88?2.60a
138 (38.55)
2.22?0.64a
273 (76.26)a
2.88?0.78a
106 (29.61)a
1.49?0.15a
5 (1.40)
1.06?0.20a
116 (32.40)a
1.47?0.43a
11 (3.07)a
Hypertension (n¼257)
52.19?13.51a,b
164/93a,b
2.56?1.03a,b
38.33?12.64
154.64?8.70c,d
50.51?8.09
21.01?1.95
13 (5.06)c,b
73.15?6.56d
156 (60.70)d
90 (35.02)
8874?327a
292.34?21.56a
79.38?7.89a,b
60.75?6.87a,b
189.63?116.32
7.81?3.24a,b
8.58?2.87a,b
146.56?15.46a,b
88.07?10.38a,b
58.49?17.10a,b
114 (44.36)
39 (15.18)
104 (40.47)
4.30?0.52a,b
0
0.91?0.28b
0
2.13?0.48a,d
180 (70.04)
2.15?0.44b
0b
1.44?0.15a,b
2 (0.78)
0.84?0.14c,b
1 (0.39)b
1.80?0.50b
8 (3.11)a
Both hyperlipidemia and hypertension (n¼189)
53.31?13.70a,b
123/66a,b
2.38?0.92a,b
38.76?12.33
154.84?8.22c,d
51.65?8.68c
21.42?2.63
36 (19.05)a,e
75.58?8.31a,e
119 (62.97)c,d
79 (41.80)a,b
8758?279b,e
290.22?20.27a
80.32?7.92a,b
63.45?7.28a,e
193.26?102.39
7.73?2.88a,b
8.75?3.08a,b
148.74?16.08a,b
87.56?11.61a,b
61.19?16.79a,b,f
87 (46.03)
27 (14.29)
75 (39.68)
5.50?1.24a,e
141 (74.60)
2.30?3.40a,b,e
83 (43.93)
2.31?0.74a,e
157 (83.07)a,e
2.56?0.83a,b,e
46 (24.34)a,e
1.49?0.18a,e
3 (1.59)
1.00?0.24a,b,e
45 (23.81)a,e
1.83?1.97b
14 (7.41)d,f
Age (years)
Men/women
Education level (years)
Physical activity (h/week)
Height (cm)
Weight (kg)
BMI (kg/m2)
>24 kg/m2[n (%)]
Waist circumference (cm)
Alcohol consumption [n (%)]
Cigarette smoking [n (%)]
Energy (kJ/day)
Carbohydrate (g/day)
Protein (g/day)
Total fat (g/day)
Dietary cholesterol (mg/day)
Total dietary fiber (g/day)
Salt intake (g/day)
SBP (mmHg)
DBP (mmHg)
Pulse pressure (mmHg)
Isolated SBP?140 mmHg [n (%)]
Isolated DBP?90 mmHg [n (%)]
Both SBP and DBP high [n (%)]
Serum total cholesterol (mmol/l)
>5.17 mmol/l [n (%)]
Triglyceride (mmol/l)
>1.70 mmol/l [n (%)]
HDL-C (mmol/l)
>1.81 mmol/l [n (%)]
LDL-C (mmol/l)
>3.20 mmol/l [n(%)]
Apolipoprotein A1 (g/l)
<1.0 g/l [n (%)]
Apolipoprotein B (g/l)
>1.14 g/l [n (%)]
Apolipoprotein A1/B
>2.50 [n (%)]
42.23?14.74
397/468
4.96?1.79
37.37?13.12
153.30?7.74
49.78?7.08
21.14?2.22
82 (9.48)
72.78?7.22
471 (54.45)
268 (30.98)
8773?257
365.35?26.85
53.13?6.72
40.38?5.27
178.36?105.46
10.75?3.38
7.57?2.68
116.49?10.99
73.35?8.42
43.15?10.08
0
0
0
4.15?0.63
0
0.89?0.30
0
2.03?0.39
586 (67.75)
2.10?0.52
13 (1.50)
1.41?0.13
4 (0.46)
0.81?0.16
4 (0.46)
1.85?0.66
72 (8.32)
DBP, diastolic blood pressure; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; SBP, systolic blood pressure.aP<0.01 compared
with normal group.bP<0.01 compared with hyperlipidemia group.cP<0.05 compared with normal group.dP<0.05 compared with hyperlipidemia group.eP<0.01
compared with hypertension group.fP<0.05 compared with hypertension group.

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results from endothelial damage may become manifested
as increased blood pressure.
Previous studies [31,32] have demonstrated that alcohol
in larger amounts influences both blood pressure and
serum lipid levels. More sodium intake for a long-term
is an important risk factor for hypertension [33–35]. The
growing prevalence of obesity is increasingly recognized
as one of the most important risk factors for the devel-
opment of hypertension. On the basis of population
studies, risk estimates indicate that at least two-thirds
of the prevalence of hypertension can be directly attri-
butedto obesity [36,37].There isalso increasing evidence
that obesity contributes to the development as well as to
theprogressionofchronickidneydisease[38,39].Obesity
might lead to hypertension and cardiovascular disease
by activating the renin–angiotensin–aldosterone system
[40], increasing sympathetic activity [41], promoting
insulin resistance and leptin resistance [42,43], potentiat-
ing procoagulatory activity [44], and inducing endothelial
dysfunction [45,46]. In the present study, however, we
found that hyperlipidemia but not hypertension was
positively correlated with BMI and alcohol consumption,
whereas hypertension but not hyperlipidemia was
Association of hyperlipidemia and hypertension Ruixing et al.
255
Table 2
Comparison of the genotypic frequencies among the four groups [n (%)]
Genotypes Normal (n¼865)Hyperlipidemia (n¼358)Hypertension (n¼257)Both hyperlipidemia and hypertension (n¼189)
PM
ACE D/I
DD
DI
II
AGT M235T
MM/MT
TT
ApoA-I C83T
CC
CT/TT
ApoB 30APOB-VNTR
HVE24-28
HVE30
HVE32
HVE34
HVE36
HVE38-64
ApoE
e2e2/e2e3
e2e4/e3e3
e3e4/e4e4
ATR2 T1334C
TT
TC/CC
CETP TaqIB
B1B1
B1B2
B2B2
GNB3 C825T
CC
CT
TT
LIPC C514T
CC
CT
TT
LPL HindIII
HþHþ
HþH?
H?H?
MTP G493T
GG
GT
TT
RGS2 G638A
GG
GA
AA
SREBP-2 G1784C
GG
GC/CC
39 (4.51)
139 (16.07)
687 (79.42)
21 (5.87)
57 (15.92)
280 (78.21)
22 (8.56)
73 (28.40)
162 (63.04)a,b
18 (9.52)
53 (28.04)
118 (62.43)a,b
0.000
345 (39.88)
520 (60.12)
139 (38.83)
219 (61.17)
103 (40.08)
154 (59.92)
74 (39.15)
115 (60.85)0.983
761 (87.98)
104 (12.02)
339 (94.69)
19 (5.31)a
242 (94.16)
15 (5.84)c
180 (95.24)
9 (4.76)c
0.000
69 (7.98)
97 (11.21)
218 (25.20)
206 (23.82)
124 (14.34)
151 (17.46)
33 (9.22)
54 (15.08)
76 (21.23)
98 (27.37)
36 (10.06)
61 (17.04)
23 (8.95)
34 (13.23)
57 (22.18)
72 (28.02)
25 (9.73)
46 (17.90)
19 (10.05)
28 (14.81)
38 (20.11)
49 (25.93)
21 (11.11)
34 (17.99) 0.384
212 (24.51)
624 (72.14)
29 (3.35)
58 (16.20)
263 (73.46)
37 (10.34)a
40 (15.57)
188 (73.15)
29 (11.28)a
27 (14.29)
142 (75.13)
20 (10.58)a
0.000
712 (82.31)
153 (17.69)
286 (79.89)
72 (20.11)
190 (73.93)
67 (26.07)c
133 (70.37)
56 (29.63)a,d
0.000
390 (45.09)
372 (43.01)
103 (11.91)
153 (42.74)
158 (44.13)
47 (13.13)
111 (43.19)
115 (44.75)
31 (12.06)
80 (42.33)
86 (45.50)
23 (12.17)0.979
224 (25.89)
424 (49.02)
217 (25.09)
87 (24.30)
180 (50.28)
91 (25.42)
60 (23.35)
126 (49.03)
71 (27.63)
43 (22.75)
95 (50.27)
51 (26.98) 0.942
251 (29.02)
484 (55.95)
130 (15.03)
105 (29.33)
195 (54.47)
58 (16.20)
78 (30.35)
136 (52.92)
43 (16.73)
53 (28.04)
103 (54.50)
33 (17.46)0.965
259 (29.94)
432 (49.94)
174 (20.12)
154 (43.02)
168 (46.93)
36 (10.06)a
114 (44.36)
114 (44.36)
29 (11.28)a
86 (45.50)
87 (46.03)
16 (8.47)a
0.000
506 (58.50)
289 (33.41)
70 (8.09)
189 (52.79)
122 (34.08)
47 (13.13)e
138 (53.70)
83 (32.30)
36 (14.01)e
100 (52.91)
61 (32.28)
28 (14.81)e
0.018
165 (19.08)
446 (51.56)
254 (29.36)
68 (18.99)
178 (49.72)
112 (31.28)
46 (17.90)
118 (45.91)
93 (36.19)
32 (16.93)
87 (46.03)
70 (37.04)0.305
684 (79.08)
181 (20.92)
278 (77.65)
80 (22.35)
201 (78.21)
56 (21.79)
146 (77.25)
43 (22.75)0.917
ACE, angiotensin-converting enzyme; AGT, angiotensinogen; ApoA-I, apolipoprotein A-I; ApoB, apolipoprotein B; ApoE, apolipoprotein E; ATR2, angiotensin receptor 2;
CETP, cholesteryl ester transfer protein; GNB3, G-protein b-3 subunit; LIPC, hepatic lipase gene; LPL, lipoprotein lipase; MTP, microsomal triglyceride transfer protein;
RGS2, Regulator of G-protein signaling 2; SREBP-2, sterol regulatory element-binding protein-2.MAdjusted values.aP<0.001 compared with normal group.bP<0.001
compared with hyperlipidemia group.cP<0.01 compared with normal group.dP<0.05 compared with hyperlipidemia group.eP<0.05 compared with normal group.