title: Renal response to angiotensin II is blunted in sodium-sensitive normotensive men.
abstract: BACKGROUND
  In hypertension, sodium sensitivity (SS) of blood pressure is associated with renal hemodynamic abnormalities related to increased activity of the renal renin-angiotensin aldosterone system (RAAS). The renal mechanisms of SS in normotensives are unknown. Therefore, we studied whether SS is related to renal hemodynamics and renal responsiveness to angiotensin II (AngII) in young healthy adults.
  
  
  METHODS
  Blood pressure (mean arterial pressure (MAP)) and renal function were measured in 34 healthy men after 1-week low-sodium diet (LS; 50 mmol Na(+)/24 h), 1-week high-sodium diet (HS; 200 mmol Na(+)/24h), and 1-week HS-ACEi (enalapril 20 mg/day). The responses of effective renal plasma flow (ERPF; (131)I-Hippuran clearance) to graded infusion of AngII were assessed during each condition.
  
  
  RESULTS
  The sodium-induced change in MAP ranged from -7 to +14 mm Hg. SS (a sodium-induced increase in MAP >3 mm Hg) was present in 13 subjects. ERPF was lower in SS subjects during LS and during HS-ACEi. The AngII-induced decrease in ERPF was blunted in SS on LS (-25 +/- 6 vs. -29 +/- 7% in sodium-resistant (SR) subjects, P < 0.05) and on HS (-30 +/- 5 vs. -35 +/- 6%, P < 0.05). The blunting was corrected by angiotensin-converting enzyme inhibitors (ACEi) (-36 +/- 6 vs. -37 +/- 7%).
  
  
  CONCLUSIONS
  SS normotensive subjects have a blunted renal response to exogenous AngII. This is ameliorated by ACEi, supporting a role for inappropriately high intrarenal RAAS activity. As these findings cannot be attributed to subclinical renal hypertensive damage, high intrarenal RAAS activity and altered renal hemodynamics may be primary phenomena underlying SS.
authors.affiliation: Department of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. f.visser@int.umcg.nl
authors.forename: Folkert W
authors.initials: FW
authors.lastname: Visser
authors.forename: Arnold H
authors.initials: AH
authors.lastname: Boonstra
authors.forename: A
authors.initials: A
authors.lastname: Titia Lely
authors.forename: Frans
authors.initials: F
authors.lastname: Boomsma
authors.forename: Gerjan
authors.initials: G
authors.lastname: Navis
mesh_terms: D000293:Adolescent; D000328:Adult; D000804:Angiotensin II / Q000494:pharmacology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D018592:Cross-Over Studies; D004656:Enalapril / Q000494:pharmacology; D006801:Humans; D007668:Kidney / Q000098:blood supply* / Q000187:drug effects* / Q000502:physiology; D008297:Male; D011673:Pulsatile Flow / Q000502:physiology; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D012964:Sodium / Q000494:pharmacology*; D012982:Sodium, Dietary / Q000494:pharmacology; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D012982:Sodium, Dietary; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D004656:Enalapril; D012964:Sodium