Key result
A 5-day low-sodium diet decreased baseline cardiac output (from 6.4 to 5.5 L/min, P=0.003) and increased peripheral resistance in healthy Gly16 homozygotes, but not in Arg16 homozygotes.
Why the study?
Does dietary sodium restriction modulate beta2-adrenergic receptor-mediated cardiovascular responses differently in healthy Gly16 versus Arg16 homozygotes?
Does dietary sodium restriction modulate beta2-adrenergic receptor-mediated cardiovascular responses differently in healthy Gly16 versus Arg16 homozygotes?
Absolute Event Rate: 5.5% vs 6.4%
p-value: p=0.003
Dietary sodium restriction blunts the enhanced beta2-adrenergic receptor responsiveness typically seen in Gly16 homozygotes, demonstrating a significant gene-environment interaction in cardiovascular regulation.
Low-Na+ diet blunts Gly16-enhanced beta2AR vasodilation; leaves open whether genotype-specific sodium effects alter clinical outcomes.
Dietary Na+ intake influences beta2-adrenergic receptor (beta2AR) responsiveness. While receiving a normal Na+ diet (150 mmol day(-1)), subjects homozygous for glycine at amino acid 16 (Gly16) have greater forearm beta2AR-mediated vasodilatation than subjects homozygous for arginine (Arg16), an effect that is mediated by endothelial NO. We tested the hypothesis that dietary Na+ restriction eliminates genotype differences in forearm and systemic beta2AR-mediated dilatation in these groups. We measured heart rate, mean arterial pressure and cardiac output (CO, acetylene breathing) responses to administration of intravenous terbutaline (TRB) before and after 5 days of low dietary Na+ intake (10 mmol day(-1)) in healthy Gly16 (n = 17; age, 31 +/- 7 year) and Arg16 homozygotes (n = 15; age, 29 +/- 8 year). After the low-Na+ diet, a catheter was placed in the brachial artery to measure forearm blood flow (FBF, plethysmography) responses to administration of isoprenaline (isoproterenol) before and after NO inhibition with NG-mono-methyl-L-arginine (L-NMMA). In the Gly16 group, the low-Na+ diet decreased baseline CO from 6.4 +/- 1.4 to 5.5 +/- 1.2 l min(-1) (P = 0.003, paired t test), tended to decrease stroke volume from 97.0 +/- 20.6 to 86.9 +/- 21.7 ml (P = 0.06) and increased peripheral resistance from 1106 +/- 246 to 1246 +/- 222 dynes s cm(-5) (P = 0.02); significant effects of the low-Na+ diet were not observed in Arg16 subjects. In a repeated measures ANOVA, the responses of all cardiovascular measures to systemic administration of TRB were not influenced by genotype or diet. Additionally, the FBF response to incremental doses of isoprenaline did not differ between genotype groups before or after administration of L-NMMA. We conclude that dietary Na+ restriction blunted the increased forearm NO-mediated beta2AR responsiveness in Gly16 homozygotes observed in a previous study after normal dietary Na+ intake, while baseline CO decreased and peripheral resistance increased in this group. This study provides evidence that dietary Na+ modulates effects of the Arg16Gly polymorphism on cardiovascular function.
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Eisenach et al. (2006) studied Healthy subjects (n=32). Low dietary sodium intake vs. Normal dietary sodium intake (baseline) was evaluated on Baseline cardiac output in Gly16 homozygotes (p=0.003). A 5-day low-sodium diet decreased baseline cardiac output (from 6.4 to 5.5 L/min, P=0.003) and increased peripheral resistance in healthy Gly16 homozygotes, but not in Arg16 homozygotes.
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