title: Dietary sodium intake modulates systemic but not forearm norepinephrine release.
abstract: BACKGROUND
  Sodium intake has profound effects on systemic and renal sympathetic activity, but its effects on sympathetic activity in skeletal muscle vascular beds, a site at which local regulatory mechanisms could alter vascular tone directly, are unclear.
  
  
  METHODS
  To determine the effect of dietary sodium intake on basal and isoproterenol-stimulated systemic and forearm norepinephrine kinetics, we studied seven healthy male volunteers twice, 4 weeks apart, while they were receiving a low-sodium (10 mmol sodium/24 hours) diet and a high-sodium diet (250 mmol sodium/24 hours). Forearm blood flow, measured by plethysmography, and systemic and forearm norepinephrine spillover, measured by radioisotope dilution, were determined before and after intra-arterial infusion of 60 and 400 ng/min isoproterenol.
  
  
  RESULTS
  Baseline (before isoproterenol) systemic norepinephrine spillover was higher when subjects received the low-sodium diet (448.1 +/- 55.7 ng/min) compared with the high-sodium diet (269.7 +/- 42.7 ng/min; p < 0.05). In contrast, sodium intake did not affect local forearm norepinephrine spillover, either at baseline (low-sodium diet, 2.05 +/- 0.48 ng/min versus high-sodium diet, 2.63 +/- 0.79 ng/min; p = 0.50) or after stimulation with isoproterenol in doses of 60 ng/min (low-sodium diet, 8.84 +/- 2.2 ng/min versus high-sodium diet, 6.1 +/- 1.9 ng/min; p = 0.38) or 400 ng/min (low-sodium diet, 16.4 +/- 4.5 ng/min versus high-sodium diet, 16.7 +/- 2.5 ng/min; p = 0.93).
  
  
  CONCLUSIONS
  Under conditions of low sodium intake, systemic norepinephrine spillover was increased but forearm norepinephrine spillover was not, suggesting that alteration in sodium intake may produce a differential effect on norepinephrine spillover in different tissues but that decreased local sympathetic activity in skeletal muscle is not the likely mechanism by which a low-sodium diet may lower blood pressure or attenuate stress-induced pressor responses.
authors.affiliation: Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232-6602, USA.
authors.forename: C M
authors.initials: CM
authors.lastname: Stein
authors.forename: R
authors.initials: R
authors.lastname: Nelson
authors.forename: M
authors.initials: M
authors.lastname: Brown
authors.forename: H
authors.initials: H
authors.lastname: He
authors.forename: M
authors.initials: M
authors.lastname: Wood
authors.forename: A J
authors.initials: AJ
authors.lastname: Wood
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000328:Adult; D004305:Dose-Response Relationship, Drug; D005542:Forearm / Q000098:blood supply*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism*; D010991:Plethysmography / Q000187:drug effects; D012982:Sodium, Dietary / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D000318:Adrenergic beta-Agonists; D012982:Sodium, Dietary; D007545:Isoproterenol; D009638:Norepinephrine