• hypertension;
  • blood pressure;
  • association study


  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References
  9. Appendix

The aim of this study was to investigate the association between polymorphisms in the β2-adrenergic receptor gene (ADRB2) (−47C/T, Arg16/Gly, Gln27/Glu) and stage-2 hypertension in northern Han Chinese. We recruited 503 individuals with stage-2 hypertension and 504 age-, gender-, and area-matched controls from the International Collaborative Study of Cardiovascular Disease in Asia. Genotyping was performed using PCR-RFLP. Logistic regression analyses revealed that carriers of the Gly16 allele had a significantly higher odds ratio (OR) for hypertension, while carriers of the Glu27 allele had a significantly lower OR. In multivariate linear regression analyses, the Arg16/Gly and Gln27/Glu genotypes were significantly associated with systolic blood pressure level (p= 0.004 and p < 0.001, respectively). In haplotype analyses, we found the frequency of haplotypes composed of the Gly16 and Gln27 alleles was significantly higher, whereas the frequency of haplotypes composed of the Arg16 and Glu27 alleles was significantly lower, in hypertensives compared to their controls (both p= 0.001). These results indicate that the Gly16 and Gln27 alleles of the ADRB2 gene confer an increased risk for stage-2 hypertension in this northern Han Chinese population.


  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References
  9. Appendix

The β2-adrenergic receptor has been implicated in the pathogenesis of hypertension, both on the basis of studies suggesting altered β2- mediated changes of cardiovascular functions (Insel, 1996; Skrabal et al. 1989; Lefkowitz et al. 1997) and on the basis of molecular genetic studies (Krushkal et al. 1998; Bray et al. 2000; Kotanko et al. 1997). Three polymorphisms in the ADRB2 gene have been reported and studied: −47C/T, Arg16/Gly and Gln27/Glu. Among these variations, the Gly16 allele of the Arg16/Gly polymorphism has been ascribed a greater degree of agonist–induced downregulation of ADRB2 in transfected fibroblasts and human bronchial smooth muscle (Liggett, 1999). But in human adipocytes, the Gly16 allele was also related to a 5-fold increased sensitivity to catecholamine–induced lipolysis (Large et al. 1997). In African Caribbeans (Kotanko et al. 1997) and Austrians (Gratze et al. 1999), the Gly16 allele has been associated with hypertension or elevated blood pressure. However, Bengtsson et al. (2001) recently found an association between the Arg16 allele and hypertension in subjects with type 2 diabetes from Sweden. In the offspring of Norwegians (Timmermann et al. 1998) and Germans (Busjahn et al. 2000), carriers of the Arg16 allele have also been found to have higher blood pressure. The Gln27/Glu polymorphism has also been variably associated with hypertension or blood pressure levels in several studies (e.g. Bengtsson et al. 2001; Busjahn et al. 2000). However, contrary to these positive results that associated the ADRB2 polymorphisms with hypertension or blood pressure regulation, a recent combined linkage and association study performed in Poland did not support a role for the ADRB2 gene as a major cause of the linkage for hypertension detected in the 5q31.1 – 5qter region (Tomaszewski, 2002).

In populations of Asian origin, findings are inconsistent. Kato et al. (2001) showed that the ADRB2 polymorphisms were unlikely to confer principal genetic susceptibility for hypertension in a Japanese population. However, in a population of Chinese origin, primarily from Taiwan, the San Francisco Bay area and Hawaii, Ranade et al. (2001) found a significant association between the Gly16 allele and hypertension. The aim of this study was to investigate whether the −47C/T, Arg16/Gly, and Gln27/Glu polymorphisms in the ADRB2 gene were associated with hypertension in northern Han Chinese, who have been proven to have significantly higher incidence and prevalence rates of cardiovascular diseases, including hypertension and higher mean levels of blood pressure (Wu et al. 1995).

Materials and Methods

  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References
  9. Appendix


All the DNA samples and clinical data for participants in this study were collected from the International Collaborative Study of Cardiovascular Disease in Asia (InterASIA in China) (Gu et al. 2002). The protocol was approved by the local bioethical committee and informed consent was obtained from each participant. InterASIA selected a nationally representative sample of the general population aged 35 to 74 years in China. A total of 15,838 persons completed the survey and examination (Gu et al. 2002). Among these, we enrolled 503 unrelated stage-2 hypertensive patients and 504 unrelated healthy control subjects from three northern field centres of InterASIA, namely Jilin, Beijing and Shandong, with a high prevalence of cardiovascular morbidity and mortality. Three BP measurements were obtained from each participant by trained and certified observers, according to a standard protocol recommended by the American Heart Association (Perloff et al. 1993). Hypertension was defined as an average systolic BP (SBP) ≥ 140 mmHg, an average diastolic BP (DBP) ≥ 90 mmHg, and/or self-reported current treatment for hypertension with antihypertensive medication. Stage-2 hypertension was defined as an average SBP ≥ 160 mm Hg and/or DBP ≥ 100 mm Hg (Chobanian et al. 2003). The control subjects had systolic and diastolic blood pressures < 140 mm Hg and < 90 mm Hg, respectively. Subjects with secondary hypertension, coronary heart disease and diabetes were excluded from the study. All hypertensive subjects meeting the above criteria at the three field centres were recruited into this study. Normotensive controls were randomly selected and matched for age, gender, and area of residence.

Blood pressure values from subjects remaining on antihypertensive medications were nonparametrically adjusted for treatment effects according to the algorithm used in analyses of Framingham data (Levy et al. 2000). Briefly, the adjustments were based on an algorithm using the expected value of the untreated residue, conditioned on the distribution of the other residuals of equal or greater magnitude, as the adjusted residual for a treated observation. Adjusted blood pressure was then achieved by adding the difference between the adjusted residual and the initial residual to the measured blood pressure value. Separate adjustments were conducted for men and women. Cubic regression models were fitted to account for age effects, and then residuals were sorted from largest to smallest within age groups (35 to 44, 45 to 54, 55 to 64, 65 to 74). Adjustment for treatment effect proceeded within each age group. Let r(k) denote the kth residual sorted in descending order; let BP(k) denote the recorded BP and let h(k) = 1 if the observation was treated, 0 otherwise. For k= 1 to n, the adjusted residual can be computed as follows: r*(k) =[1-h(k)]r(k)+h(k){[r(k)+Σr*(j)]/k}, with summation from j= 1 to k− 1. Adjusted BP is computed as BP*(k) =BP(k)+r*(k)-r(k). (Levy et al. 2000) Observations from individuals not taking antihypertensive medications remained unchanged.

Genotyping and Statistical Analysis

We genotyped the −47C/T, Arg16/Gly, and Gln27/Glu polymorphisms in the ADRB2 gene by means of polymerase chain reaction and restriction fragment-length polymorphism methods, as described elsewhere (Bengtsson et al. 2001; McGraw et al. 1998).

Statistical analyses were conducted using the SAS program, 2LD program and EH/EH+ program ( (Xie et al. 1993; Zapata et al. 2001; Zhao et al. 2000). Hardy-Weinberg equilibrium was assessed using the χ2 test and the FINETTI program (

Continuous variables by hypertension status are presented as mean ± SD. Univariate analysis to measure the association of each single polymorphism with stage-2 hypertension was performed by the χ2 test. The association between genotypes and hypertension was analyzed by stepwise logistic regression and expressed as an odds ratio (OR) with a 95% confidence interval (CI). Multivariate analysis to test the association between genotypes and blood pressure levels was conducted by stepwise multiple linear regression and ANCOVA. Pairwise linkage disequilibrium coefficients were calculated with estimated haplotype frequencies using the 2LD program. The extent of disequilibrium was expressed in terms of D′. Haplotype frequencies for various polymorphism combinations were estimated using the EH/EH+ program. The EH/EH+ program also performed an omnibus likelihood ratio test to examine the differences in haplotype frequency profiles between the cases and the controls (Zhao et al. 2000). All statistical tests were 2-tailed, and p < 0.05 was considered statistically significant.


  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References
  9. Appendix

Clinical Characteristics

Of the 503 hypertensive subjects, 166 (33.0%) remained on the antihypertensive therapy during the two weeks prior to the interview. The demographic and clinical data from all individuals are shown in Table 1. Aside from blood pressure measurements and BMI, serum cholesterol, triglyceride, glucose and creatinine levels were significantly higher in cases than in controls. There were no significant differences between the cases and controls for smoking and drinking status.

Table 1.  Comparison of clinical characteristics between cases and controls
 Cases (n = 503)Controls (n = 504) P
  1. Values are mean ± SD. NS indicates not significant; SBP, systolic blood pressure; DBP, diastolic blood pressure; BMI, body mass index; TC, total cholesterol; HDL-C, HDL cholesterol; LDL-C, LDL cholesterol; TG, triglyceride; Glu, glucose; Cr, creatinine; Smokers, the number of cigarette consumers who has smoked not less than 100 cigarettes; Drinkers, the number of alcohol consumers who drank not less than 12 times during the year ahead of the interview.

Gender, M/F262/241263/241NS
Age, y53.57 ± 9.3453.67 ± 9.18NS
SBP, mm Hg177.07 ± 28.05117.58 ± 11.65<0.001
DBP, mm Hg104.34 ± 12.2875.08 ± 7.96<0.001
BMI, kg/m226.32 ± 3.8524.34 ± 3.57<0.001
TC, mmol/L5.23 ± 0.995.07 ± 1.040.01
HDL-C, mmol/L1.25 ± 0.301.32 ± 0.34<0.001
LDL-C, mmol/L3.19 ± 0.863.09 ± 0.86NS
TG, mmol/L1.70 ± 1.061.42 ± 0.85<0.001
Glu, mmol/L5.93 ± 1.795.57 ± 1.660.001
Cr, μmol/L71.22 ± 14.5969.14 ± 11.510.01

Association Analyses

Table 2 shows the genotype frequencies for 3 polymorphisms in the ADRB2 gene in northern Han Chinese. Univariate analyses indicated that the Arg16/Gly and Gln27/Glu polymorphisms were significantly associated with stage-2 hypertension. The frequencies of the Gly16 allele and Gln27 allele were significantly higher in cases than in controls. In the stepwise logistic regression analysis, there was a significant increase in the OR (OR = 1.46; 95% CI, 1.11 to 1.93) for hypertension in the Gly16 allele carriers, whereas the OR (OR = 0.42, 95% CI, 0.28 to 0.62) in the Glu27 allele carriers was decreased. BMI, serum triglyceride, creatinine and glucose levels were also associated with hypertension by the logistic regression analysis with the Arg16/Gly and Gln27/Glu genotypes as independent variables.

Table 2.  Genotype frequencies of 3 ADRB2 polymorphisms
GenotypeCases (n = 503) Total [M/F]Controls (n = 504) Total [M/F] P
  1. NS indicates not significant.

 C/C6 [2/4]6 [5/1] 
 C/T97 [51/46]102 [54/48] 
 T/T400 [209/191]396 [204/192]NS
 Frequency of C allele (%)10.8 [10.5/11.2]11.3 [12.2/10.4]NS
 Gly/Gly106 [55/51]86 [51/35] 
 Gly/Arg236 [126/110]217 [115/102] 
 Arg/Arg161 [81/80]201 [97/104]0.026 [NS/0.04]
 Frequency of Gly Allele (%)44.5 [45.0/44.0]38.6 [41.3/35.7]0.007 [NS/0.008]
 Glu/Glu8 [4/4]6 [5/1] 
 Glu/Gln39 [21/18]88 [49/39] 
 Gln/Gln456 [237/219]410 [209/201]0.001 [0.001/<0.001]
 Frequency of Glu Allele (%)5.5 [5.5/5.4]9.9 [11.2/8.5]0.001 [0.001/0.057]

In the stepwise multiple linear regression analyses, we found that the Gly16 allele and Gln27 allele were significantly associated with systolic blood pressure level (p= 0.004 and p < 0.001, respectively). BMI, serum glucose levels, drinking status, serum creatinine and triglyceride levels were accepted into the final regression model (all the p values < 0.05). The Gln27 allele was found to have a significant association with diastolic blood pressure (p < 0.001), whereas the significance of the association between the Gly16 allele and diastolic blood pressure was marginal (p= 0.05) after adjusting for other conventional risk effects. To further examine the association between the ADRB2 genotypes and blood pressure levels, we analyzed the mean values according to the ADRB2 genotypes by ANCOVA (Table 3). We also performed multiple linear regression analyses for systolic and diastolic blood pressures without adjustment for treatment status. The association of the Gly16 allele and Gln27 allele with systolic blood pressure level remained significant (p= 0.01 and p < 0.001, respectively). For diastolic blood pressure, the results also tended to be consistent with analyses of adjusted blood pressure values (p < 0.001 for the Gln27 allele, while the Gly16 allele was not significant).

Table 3.  Differences in clinical characteristics for the Arg16/Gly and Gln27/Glu polymorphisms
  1. Values are mean ± SD. The mean values were adjusted and compared by ANCOVA. NS indicates not significant; SBP, systolic blood pressure; DBP, diastolic blood pressure; BMI, body mass index; Cr, creatinine; Glu, glucose.

n, subjects192453362 
SBP, mm Hg150.25 ± 36.26149.49 ± 36.61142.98 ± 36.730.025
DBP, mm Hg 91.19 ± 17.61 90.24 ± 18.03 88.22 ± 17.89NS
BMI, kg/m2 25.41 ± 3.59 25.44 ± 3.94 25.15 ± 3.84<0.001
Cr, μmol/L 70.08 ± 12.77 70.31 ± 13.33 70.08 ± 13.220.01
Glu, mmol/L  5.75 ± 1.40  5.70 ± 1.52  5.81 ± 2.11<0.001
Glu/Glu + Glu/GlnGln/Gln
n, subjects141866 
SBP, mm Hg136.25 ± 30.45149.09 ± 37.32<0.001 
DBP, mm Hg 84.39 ± 17.55 90.56 ± 17.84<0.001 
BMI, kg/m2 25.05 ± 3.62 25.38 ± 3.88<0.001 
Cr, μmol/L 70.76 ± 16.95 70.08 ± 12.43 0.008 
Glu, mmol/L  5.87 ± 2.38  5.73 ± 1.61<0.001 

There was significant linkage disequilibrium between the −47C/T and Arg16/Gly polymorphism (D′= 0.66, p < 0.001). The linkage disequilibrium for the other two polymorphism combinations (i.e., Arg16/Gly − Gln27/Glu and −47C/T − Gln27/Glu) was weaker, but also significant (D′= 0.36 and 0.33, respectively, p < 0.001). Figure 1 presents the distributions of the −47C/T as well as the Gln27/Glu polymorphisms that were significantly associated with the distribution of the Arg16/Gly polymorphism. The genotypes homozygous for Glu27/Glu and −47C/C tended almost always to be associated with the Gly16/Gly genotype, and the frequency of the −47T allele appeared to increase significantly from non-Arg16 allele carriers to homozygous Arg16/Arg carriers (p= 0.001).


Figure 1. Distributions of the −47C/T and Gln27/Glu Genotypes according to the Arg16/Gly Genotype.

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Haplotype analyses

Table 4 shows the results of the haplotype analyses for various polymorphism combinations. For all four combinations, omnibus haplotype profile tests showed significant associations with stage-2 hypertension in this population. Univariate analysis for 2-polymorphism combinations showed that the frequency of haplotypes composed of the Gly16 and Gln27 allele was significantly higher, while the frequency of haplotypes composed of the Arg16 and Glu27 allele was lower in the cases than in the controls (both p= 0.001), indicating the haplotypes with the Gly16 and Gln27 alleles were associated with hypertension. This result was consistent with the individual polymorphism analyses. In the univariate analysis for the 3-polymorphism combination, haplotype containing block of Gly16, Gln27 along with the −47T allele was found to be associated with hypertension (p= 0001 and 0.002, respectively).

Table 4.  Estimates for haplotype frequencies and comparison between cases and controls
Polymorphism CombinationsHaplotypeOverallCasesControlsχ2dfP
  1. *Likelihood ratio statistic for omnibus test in EH program.

−47C/TT – Arg0.5200.4950.545  4.97 10.026
Arg16/GlyT – Gly0.3700.3970.342  6.39 10.011
 C – Arg0.0640.0600.069  0.80 1NS
 C – Gly0.0460.0480.044  0.19 1NS
 Ln (L)*−1582.33−785.74−792.04  9.10 3<0.05
Arg16/GlyArg – Gln0.5390.5250.553  1.56 1NS
Gln27/GluGly – Gln0.3840.4210.348 11.41 10.001
 Arg – Glu0.0450.0300.061 11.00 10.001
 Gly – Glu0.0320.0240.038  3.23 1NS
 Ln (L)−1507.39−711.17−784.29 23.86 3<0.01
−47C/TT – Gln0.8210.8430.799  6.73 10.01
Gln27/GluC – Gln0.1020.1020.102  0.00 1NS
 T – Glu0.0680.0490.088 12.36 10.001
 C – Glu0.0090.0060.011  1.47 1NS
 Ln (L)−978.09−450.43−519.52 16.28 3<0.01
−47C/TT – Arg – Gln0.5200.4680.491  1.06 1NS
Arg16/GlyT – Gly – Gln0.2820.3750.308 10.12 10.001
Gln27/GluC – Arg – Gln0.0730.0570.063  0.4161NS
 T – Arg – Glu0.0490.0270.054  9.32110.002
 C – Gly – Gln0.0390.0460.039  0.6161NS
 T – Gly – Glu0.0260.0220.034  2.6211NS
 C – Arg – Glu0.0070.0030.0071NS
 C – Gly – Glu0.0040.0020.0041NS
 Ln (L)−1739.56−957.96−1025.98488.76 7<0.01


  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References
  9. Appendix

One key finding of the present study was the increased risk for hypertension and higher systolic blood pressure in the carriers of the Gly16 allele of the ADRB2 gene in a northern Han Chinese population. This finding, is interestingly in opposition to some reports from several populations supporting the Arg16 allele as a potential risk factor for hypertension (Table 5). However, some other results support our findings. Firstly, an association between the Gly16 allele and hypertension was reported in African Caribbeans (Kotanko et al. 1997). Black Americans are known to be more salt sensitive than whites (Luft et al. 1997). Thus, there is a hypothesis that the Gly16 allele might be associated with salt sensitivity, and this has been proposed to explain the association between hypertension and the Gly16 allele in African Caribbeans (Kotanko et al. 1997). Secondly, the Gly16 allele has been shown to result in less propensity to vasodilation in response to salbutamol infusion in normotensive white subjects from Austria (Gratze et al. 1999). However, in contrast to all these studies, several reports on Japanese (Kato et al. 2001), Europeans (Tomaszewski et al. 2002), white and African Americans (Herrmann et al. 2000) did not support the Arg16/Gly polymorphism in the ADRB2 gene as a principal susceptibility variant for hypertension. Ethnic differences might be partially responsible for the observed discrepancy and the hypertension risk profile. Hypertensive mechanisms might not be the same not only among people of different origin, such as black Americans, whites and Asians, but also within a similar population, e.g. Caucasians. It is also likely that low power may account for some discrepancies among other studies. However, there is an alternative possibility that it is not the Arg16/Gly polymorphism per se but rather some polymorphism in linkage disequilibrium with the Arg16/Gly polymorphism, that is responsible for the association (Bengtsson et al. 2001). Furthermore, we have also found an association of the Gln27 allele of the ADRB2 gene with hypertension in this northern Han Chinese population, as reported in a European population previously (Bengtsson et al. 2001), but not confirmed in other Chinese populations from Taiwan, the San Francisco Bay area and Hawaii (Ranade et al. 2001).

Table 5.  Comparison of major results from studies of the ADRB2 polymorphisms in different populations
Study PopulationSample SizeTraits TestedAssociated AllelesReferences
  1. HT indicates hypertensive/hypertension; NT, normotensive; NS, not significant; NE, not examined; BP, blood pressure; SBP, systolic blood pressure; 2-DM, type 2 diabetes mellitus.

African Caribbean136 HT, 81 NTHTGly16NSKotanko et al. 1997
Austrian57 NTBPGly16NEGratze et al. 1999
Non-Hispanic Whites644 familiesHT; BPGly16Glu27Bray et al. 2000
Southern Chinese595 HT, 264 NTHTGly16NSRanade et al. 2001
Northern Han Chinese503 HT, 504 NTHT; BPGly16Gln27-
Norwegian23 HT families,HT; BPArg16NSTimmermann et al. 1998
 22 NT families 
German166 NT twinsSBPArg16Glu27Busjahn et al. 2000
Swede124 HT+2-DMHT+ 2-DM;Arg16Gln27Bengtsson et al. 2001
 291 HT, 265 NT;BP 
 112 NT sib pairs 
Japanese842 HT, 633 NT,HTNSNSKato et al. 2001
 525 DM 
Polish210 familiesHTNSNSTomaszewski et al. 2002

The haplotype analysis produced important information about the respective and combined effects of the three polymorphisms tested. We found the estimated frequencies of haplotypes containing the Gly16 and Gln27 alleles (Gly16-Gln27 and T-Gly16-Gln27) were significantly higher in the cases than in the controls. Haplotype analysis can provide more information than analysis with a single polymorphic marker. In our data, haplotype analysis confirmed the findings from the simple analysis.

In our analyses, we adjusted the blood pressure levels for treatment effect using the algorithm in the analyses of Framingham data (Levy et al. 2000). This might be potentially hazardous, because in any treated group of hypertensives the response to medications might differ. Therefore, we also analyzed the data with the unadjusted blood pressure values to reduce any potential confounding effect. The results were in accordance with what we obtained using the adjusted data on the whole.

A significant deviation from the Hardy-Weinberg equilibrium (HW-E) was detected for the Arg16/Gly polymorphism for controls and the Gln27/Glu polymorphism for cases (p= 0.04 and p < 0.001, respectively), which prompted us to test the HW-E of genotype frequencies from other studies for these two polymorphisms. We found the same excess of homozygous individuals for the Arg16/Gly polymorphism as in a study performed using German subjects (Busjahn et al. 2000). This similar deviation could also be observed in healthy subjects (Turki et al. 1995), and healthy as well as hypertensive persons (Kotanko et al. 1997). In another population of southern Chinese origin, the distributions of the Arg16/Gly and Gln27/Glu polymorphisms also showed significant deviations from the HW-E in the same direction in healthy subjects (Ranade et al. 2001). Table 6 summarizes these reported deviations. This phenomenon and the fact that the distribution of the −47C/T genotypes in the same gene was in accordance with the HW-E in these studies may not indicate that these deviations from the HW-E were directly due to genotyping error. We have retyped these polymorphisms independently and ensured the genotyping error is not significant.

Table 6.  Deviations from Hardy-Weinberg Equilibrium for the Arg16/Gly and Gln27/Glu polymorphisms in different studies
Study PopulationAffected StatusPolymorphismsN, subjects (%)PReferences
  1. NT indicates normotensive; HT, hypertensive.

AfricanNTArg16/Gly Kotanko et al. 1997
Caribbean Gly/Gly 42 (51.9) 
 Gly/Arg 24 (29.6) 
 Arg/Arg 15 (18.5)0.003 
 Gly/Gly101 (74.3) 
 Gly/Arg 28 (20.6) 
 Arg/Arg  7 (5.1)0.02 
GermanNT TwinsArg16/Gly Busjahn et al. 2000
 Gly/Gly 71 (33.3) 
 Gly/Arg 84 (39.5) 
 Arg/Arg 58 (27.2)0.002 
SouthernNTArg16/Gly Ranade et al. 2001
Chinese Gly/Gly 55 (20.8) 
 Gly/Arg110 (41.7) 
 Arg/Arg 99 (37.5)0.02 
 Glu/Glu  5 (1.9) 
 Glu/Gln 37 (14.1) 
 Gln/Gln220 (84.0)0.04 
NorthernNTArg16/Gly -
Han Chinese Gly/Gly 86 (17.1) 
 Gly/Arg217 (43.0) 
 Arg/Arg201 (39.9)0.04 
 Glu/Glu  8 (1.6) 
 Glu/Gln 39 (7.8) 
 Gln/Gln456 (90.6)<0.001 

In summary, we examined three polymorphisms of the ADRB2 gene in an extensive association study within a population of northern Han Chinese. The Gly16 and Gln27 alleles conferred an increased risk for stage-2 hypertension. This association was partially supported by the findings from a population of southern Chinese origin (Ranade et al. 2001). Further investigation is warranted to elucidate the relationship between the ADRB2 polymorphisms and hypertension in a variety of ethnic groups.


  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References
  9. Appendix

This work was funded by grants 2001AA227081, Z19-01-03-01 of the National High Technology Research and Development Program, grants 2002BA711A05, 2002BA711A08 of the National Tenth Five-year Plan Key Program from the Ministry of Science and Technology of the People's Republic of China, and grants H010210370113, H020220030130 biomedical projects from the Council of Science and Technology, Beijing.


  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References
  9. Appendix
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