title: Sodium intake is associated with parasympathetic tone and metabolic parameters in mild hypertension.
abstract: BACKGROUND
  Although the impairment of parasympathetic cardiac control was described in hypertensives submitted to a high salt diet, the impact of this autonomic abnormality on metabolic and inflammation markers in patients with mild hypertension has not been explored.
  
  
  METHODS
  Four hundred and ninety mild essential hypertensive patients (144 ± 9/94 ± 9 mm Hg, 49.5 ± 13.9 years, 67.9 % male) were studied. Dietary sodium intake was estimated by measuring 24-h urinary sodium excretion (UNa), and the patients were classified according to UNa levels as follows: low (<50 mEq/l), medium (50-99 mEq/l), and high UNa (≥100 mEq/l). Parasympathetic tone was evaluated by assessing heart rate recovery (HRR) after an exercise stress test. HRR, plasma lipids, glucose metabolism, and inflammatory biomarkers were compared across UNa groups.
  
  
  RESULTS
  HRR and high-density lipoprotein (HDL)-cholesterol were progressively lower, and insulin (INS), homeostasis model assessment of insulin resistance (HOMAir), ultrasensitive-C-reactive protein (usCRP) were progressively higher across increasing UNa groups. In the low and medium UNa groups, HDL-cholesterol was higher and CRP was lower than that in high UNa (P < 0.01 and P < 0.05, respectively) (Dunnett post-hoc test). In the low UNa group, triglycerides (TGs), INS, and HOMAir were lower than that in high UNa (P < 0.05). Multiple linear regression analysis showed that UNa, HOMAir, and heart rate (HR) were negatively associated with HRR (P < 0.0001, P < 0.0001, and P = 0.001, respectively).
  
  
  CONCLUSIONS
  In the essential hypertensive patients studied high sodium intake is associated with parasympathetic inhibition, lipid disturbances, and inflammation. Studies designed to assess causality between sodium intake and metabolic and autonomic status are needed to evaluate the relevance of controlling sodium intake, especially in hypertensive patients.
authors.affiliation: Centro de Hipertensión Arterial, Servicio de Cardiología, Hospital Universitario Austral, Buenos Aires, Argentina. SAGONZAL@cas.austral.edu.ar
authors.forename: Sergio A
authors.initials: SA
authors.lastname: González
authors.forename: Pedro
authors.initials: P
authors.lastname: Forcada
authors.forename: Elena M V
authors.initials: EM
authors.lastname: de Cavanagh
authors.forename: Felipe
authors.initials: F
authors.lastname: Inserra
authors.forename: J Chiabaut
authors.initials: JC
authors.lastname: Svane
authors.forename: Sebastian
authors.initials: S
authors.lastname: Obregón
authors.forename: Carlos
authors.initials: C
authors.lastname: Castellaro
authors.forename: Daniel
authors.initials: D
authors.lastname: Olano
authors.forename: Alejandro
authors.initials: A
authors.lastname: Hita
authors.forename: Carol V
authors.initials: CV
authors.lastname: Kotliar
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood; D005260:Female; D005947:Glucose / Q000378:metabolism; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D010275:Parasympathetic Nervous System / Q000187:drug effects* / Q000502:physiology*; D012044:Regression Analysis; D012964:Sodium / Q000652:urine*; D012982:Sodium, Dietary / Q000494:pharmacology*
chemical_list: D008076:Cholesterol, HDL; D007328:Insulin; D008055:Lipids; D012982:Sodium, Dietary; D002097:C-Reactive Protein; D012964:Sodium; D005947:Glucose