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Physiol. Genomics (December 9, 2003). doi:10.1152/physiolgenomics.00152.2003
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Submitted on September 9, 2003
Accepted on December 2, 2003

The Arg16/Gly {beta}2-Adrenergic Receptor Polymorphism is Associated with Altered Cardiovascular Responses to Isometric Exercise

John H Eisenach1, Antonio M McGuire1, Rachel M Schwingler1, Stephen T Turner2, and Michael J Joyner1*

1 Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, MN, USA
2 Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA

* To whom correspondence should be addressed. E-mail: joyner.michael{at}mayo.edu.

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, non-obese, 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 bpm; Gly16: 65 ± 3 bpm, 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 (PANOVA = 0.001, genotype-by-time interaction). During HG, peak HR at fatigue was: Gly16: 100 ± 4 bpm (54% increase from rest) vs. Arg16: 93 ± 3 bpm (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.




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