title: Nitric oxide inhibition as a mechanism for blood pressure increase during salt loading in normotensive postmenopausal women.
abstract: OBJECTIVE
  Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO), which plays an important role in natriuresis. We determined whether changes in endothelium-dependent vasodilation (EDD) and plasma ADMA predict changes in blood pressure (BP) after salt loading in normotensive postmenopausal women (PMW).
  
  
  METHODS
  In 15 normotensive PMW (age 50-60 years), not receiving estrogen, ambulatory 24-h BP, plasma lipids, and ADMA were measured after 4 days of a low-salt diet (70 mEq/day) and following 7 days of high-salt intake (260 mEq/day). Brachial artery diameter at rest, during reactive hyperemia, i.e. EDD, and after sublingual nitroglycerin, i.e. non-EDD, were measured by ultrasound. The 24-h urinary NO metabolite (NOx) was measured by Griess reaction. Plasma ADMA was measured by high-pressure liquid chromatography.
  
  
  RESULTS
  During low-salt, 24-h BP levels averaged 121 +/- 11 and 69 +/- 7 mmHg for systolic BP (SBP) and diastolic BP (DBP), respectively. After salt loading, average 24-h BP increases were: 7.6 mmHg for SBP, 2.2 mmHg for DBP, and 5.5 mmHg for pulse pressure (PP). Increases of 24-h SBP and 24-h PP after salt loading correlated directly with changes in ADMA (partial R2 = 0.16 for 24-h SBP and 0.17 for 24-h PP, P < 0.05 for both) and inversely with changes in EDD (partial R2 = 0.13, P = 0.09 for 24 h SBP and partial R2 = 0.15, P = 0.07 for 24-h PP), after adjustment for age and cholesterol.
  
  
  CONCLUSIONS
  Inhibition of NO bioavailability by ADMA and a subsequent reduction in EDD contribute to the increase in BP during high-salt intake in normotensive PMW not receiving estrogen.
authors.affiliation: Laboratory of Cardiovascular Science, National Institute on Aging, NIH, Baltimore, Maryland, USA. angeloelefante@interfree.it
authors.forename: Angelo
authors.initials: A
authors.lastname: Scuteri
authors.forename: Markus C
authors.initials: MC
authors.lastname: Stuehlinger
authors.forename: John P
authors.initials: JP
authors.lastname: Cooke
authors.forename: Jeanette G
authors.initials: JG
authors.lastname: Wright
authors.forename: Edward G
authors.initials: EG
authors.lastname: Lakatta
authors.forename: David E
authors.initials: DE
authors.lastname: Anderson
authors.forename: Jerome L
authors.initials: JL
authors.lastname: Fleg
mesh_terms: D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D001916:Brachial Artery / Q000502:physiology; D004730:Endothelium, Vascular / Q000378:metabolism; D005260:Female; D006801:Humans; D008875:Middle Aged; D009318:Natriuresis / Q000187:drug effects / Q000502:physiology; D009569:Nitric Oxide / Q000097:blood*; D017698:Postmenopause / Q000378:metabolism*; D011237:Predictive Value of Tests; D012044:Regression Analysis; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D014664:Vasodilation / Q000502:physiology
chemical_list: D017673:Sodium Chloride, Dietary; D009569:Nitric Oxide; C018524:N,N-dimethylarginine; D001120:Arginine