Dietary sodium restriction and beta2-adrenergic receptor polymorphism modulate cardiovascular function in humans

Area of Science:

• Cardiovascular Physiology
• Pharmacology
• Nutritional Science

Background:

• Dietary sodium (Na+) intake affects beta2-adrenergic receptor (beta2AR) responsiveness.
• Individuals homozygous for glycine at amino acid 16 (Gly16) show greater beta2AR-mediated vasodilation than arginine homozygotes (Arg16) on a normal Na+ diet, mediated by endothelial nitric oxide (NO).

Purpose of the Study:

• To investigate if dietary Na+ restriction eliminates genotype differences in forearm and systemic beta2AR-mediated vasodilation.
• To determine the impact of low Na+ intake on cardiovascular responses and beta2AR function in Gly16 and Arg16 homozygotes.

Main Methods:

• Healthy Gly16 and Arg16 homozygotes underwent a 5-day low Na+ diet (10 mmol/day).
• Cardiovascular responses (heart rate, mean arterial pressure, cardiac output) to terbutaline (TRB) were measured before and after the diet.
• Forearm blood flow (FBF) responses to isoprenaline, with and without NO inhibition (L-NMMA), were assessed via brachial artery catheterization.

Main Results:

• In Gly16 subjects, low Na+ diet decreased baseline cardiac output (CO) and increased peripheral resistance, with no significant effects in Arg16 subjects.
• Systemic TRB responses were not influenced by genotype or diet.
• Forearm blood flow responses to isoprenaline did not differ between genotypes, even after NO inhibition.

Conclusions:

• Dietary Na+ restriction blunted the enhanced forearm NO-mediated beta2AR responsiveness in Gly16 homozygotes.
• Low Na+ intake altered baseline cardiovascular parameters (CO, peripheral resistance) in Gly16 individuals.
• Dietary sodium modulates the effects of the Arg16Gly polymorphism on cardiovascular function.