The Arg16/Gly β2-adrenergic receptor polymorphism is associated with altered cardiovascular responses to isometric exercise
The Arg16/Gly β2-adrenergic receptor polymorphism is associated with altered cardiovascular responses to isometric exercise
复制标题
DOI：
10.1152/physiolgenomics.00152.2003
复制
发表时间：
2004-02-13
影响因子：
4.6
通讯作者：
Joyner, MJ
中科院分区：
文献类型：
--
作者：
Eisenach, JH;McGuire, AM;Joyner, MJ
编码β 2-肾上腺素能受体的基因多态性（第16位氨基酸为精氨酸或甘氨酸）与对β 2-激动剂的血管舒张反应改变相关，这可能调节应激期间对内源性儿茶酚胺的升压反应。为了验证Arg 16/Gly多态性与交感神经兴奋引起的急性升压反应差异相关的假设，我们测量了平均动脉压，对31名健康、非肥胖、血压正常的成年人（平均年龄+/- SE：31 +/- 1; 16名女性）在精神应激（MS）、冷加压试验（CPT）和握力（HG）至疲劳期间的MAP、Finapres和心率（HR、ECG）进行了研究。受试者为Gly 16（n = 16）或Arg 16（n = 15）纯合子。两组的基线MAP（Arg 16，86 +/- 3 mmHg; Gly 16，89 +/- 2 mmHg; P = 0.4）和HR（Arg 16，68 +/- 2次/分钟; Gly 16，65 +/- 3次/分钟; P = 0.3）相似。对于MS和CPT，MAP和HR在基因型组之间没有差异。手柄也产生了类似的MAP增加，然而，在HR的变化是更大的Gly 16纯合子（P-ANOVA = 0.001，基因型与时间的相互作用）。在HG期间，Gly 16疲劳时的峰值HR为100 +/- 4次/分钟（较休息时增加54%），Arg 16为93 +/- 3次/分钟（增加37%）。我们的结论是，心血管反应MS和CPT之间没有区别Gly 16和Arg 16纯合子。然而，Gly 16纯合子对运动的更大HR反应可能有助于在该组中面对增强的外周血管舒张（降低的总外周阻力）时维持升压反应（增加的心输出量）。
A polymorphism in the gene encoding the beta(2)-adrenergic receptor (arginine or glycine at amino acid position 16) is associated with altered vasodilator responses to beta(2)-agonists, which may modulate the pressor response to endogenous catecholamines during stress. To test the hypothesis that the Arg16/Gly polymorphism is associated with differences in acute pressor responses to sympathoexcitation, we measured mean arterial pressure (MAP, Finapres) and heart rate (HR, ECG) during mental stress (MS), cold pressor test (CPT), and handgrip (HG) to fatigue in 31 healthy, nonobese, normotensive adults (mean age +/- SE: 31 +/- 1; 16 females). Subjects were homozygous for Gly16 (n = 16) or Arg16 (n = 15). Both groups had similar baseline MAP (Arg16, 86 +/- 3 mmHg; Gly16, 89 +/- 2 mmHg; P = 0.4) and HR (Arg16, 68 +/- 2 beats/min; Gly16, 65 +/- 3 beats/min; P = 0.3). For MS and CPT, MAP and HR did not differ between genotype groups. Handgrip also produced similar increases in MAP; however, the change in HR was greater in the Gly16 homozygotes (P-ANOVA = 0.001, genotype-by-time interaction). During HG, peak HR at fatigue was 100 +/- 4 beats/min for Gly16 (54% increase from rest) vs. 93 +/- 3 beats/min for Arg16 (37% increase). We conclude that the cardiovascular responses to MS and CPT do not differ between Gly16 and Arg16 homozygotes. However, the greater HR response to exercise in the Gly16 homozygotes may serve to maintain the pressor response (increased cardiac output) in the face of augmented peripheral vasodilation (decreased total peripheral resistance) in this group.