Association of the GNAS1 Gene Variant with Hypertension Is Dependent on Alcohol Consumption.

  • CHEN Yusen
    Department of Geriatric Medicine, School of Medicine, Ehime University
  • NAKURA Jun
    Department of Geriatric Medicine, School of Medicine, Ehime University
  • JIN Jing-ji
    Department of Geriatric Medicine, School of Medicine, Ehime University
  • WU Zhihong
    Department of Geriatric Medicine, School of Medicine, Ehime University
  • YAMAMOTO Miyuki
    Department of Geriatric Medicine, School of Medicine, Ehime University
  • ABE Michiko
    Department of Geriatric Medicine, School of Medicine, Ehime University
  • TABARA Yasuharu
    Department of Geriatric Medicine, School of Medicine, Ehime University
  • YAMAMOTO Yoshikuni
    Department of Geriatric Medicine, School of Medicine, Ehime University
  • IGASE Michiya
    Department of Geriatric Medicine, School of Medicine, Ehime University
  • BO Xiao
    Department of Neurology, Xiang Ya School of Medicine, Central South University
  • KOHARA Katsuhiko
    Department of Geriatric Medicine, School of Medicine, Ehime University
  • MIKI Tetsuro
    Department of Geriatric Medicine, School of Medicine, Ehime University

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抄録

The β-adrenoceptor (β-AR)-stimulatory guanine nucleotide-binding (Gs) protein system has been shown to play important roles in the cardiovascular system. The gene encoding the α-subunit of Gs proteins (GNAS1) is a candidate genetic determinant for hypertension. Because alcohol consumption is known to affect blood pressure partly through the β-AR-Gs protein system, we examined the possible interaction between GNAS1 T393C polymorphism and drinking status in the association with hypertension in the present study. As a result, a non-significant but reasonable trend supporting the presence of an interaction was shown (p =0.076). In line with this trend, the T393C polymorphism significantly interacted with drinking status in the association with systolic blood pressure (p =0.028). Moreover, supporting the presence of an interaction, T allele carriers consistently had a higher probability of hypertension, higher systolic blood pressure, and higher diastolic blood pressure than CC homozygotes in non-drinkers and light drinkers. In contrast, CC homozygotes consistently had a higher probability of hypertension, higher systolic blood pressure, and higher diastolic blood pressure than T allele carriers in moderate to heavy drinkers. The present study also showed a significant interaction between the T393C polymorphism and drinking status in the association with pulse pressure (p =0.026), reflected by a significant association between the T393C polymorphism and pulse pressure in moderate to heavy drinkers (p =0.026). These findings may be helpful in conducting further molecular and biological studies on the relationship among the effects of alcohol, the β-AR-Gs protein system, and hypertension. (Hypertens Res 2003; 26: 439-444)

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