title: Angiotensin II related to sodium excretion modulates left ventricular structure in human essential hypertension.
abstract: BACKGROUND
  Urinary sodium excretion and angiotensin II (Ang II), which are linked in a physiological feedback mechanism, have both been described to be blood pressure-independent determinants of left ventricular hypertrophy in essential hypertension. We conducted a study to investigate the interaction of sodium excretion with Ang II and its potential impact on myocardial hypertrophy.
  
  
  RESULTS
  Sixty-eight patients (46 men and 22 women; mean age, 52 +/- 10 years) with untreated World Health Organization stage I to II essential hypertension were examined in a cross-sectional study. Left ventricular structure and function (two-dimensionally guided M-mode echocardiography), dietary sodium intake (as estimated by 24-hour urinary sodium excretion), and noninvasive ambulatory blood pressure over 24 hours (Spacelab 90207) were determined in parallel with plasma renin activity and plasma Ang II and serum aldosterone concentrations (radioimmunoassay). Twenty-four-hour urinary sodium excretion emerged as a strong correlate of relative wall thickness independent of 24-hour ambulatory blood pressure (partial r = .49, P < .001). Ang II concentrations were weakly correlated with septal wall thickness (r = .27, P < .05) and left ventricular mass (r = .25, P < .05). Patients with high Ang II concentrations in relation to sodium excretion had a greater left ventricular mass (318 +/- 77 versus 257 +/- 54 g, P < .02), posterior wall thickness (11.8 +/- 1.9 versus 10.5 +/- 0.8 mm, P < .02), and septal wall thickness (13.6 +/- 1.8 versus 11.9 +/- 1.3 mm, P < .01) than those with "relatively low" Ang II levels in relation to sodium excretion.
  
  
  CONCLUSIONS
  Impaired suppression of the renin-Ang II system appeared to act as a stimulus for myocardial hypertrophy in hypertensive patients.
authors.affiliation: Department of Medicine IV/Nephrology, University of Erlangen-Nürnberg, Germany.
authors.forename: R E
authors.initials: RE
authors.lastname: Schmieder
authors.forename: M R
authors.initials: MR
authors.lastname: Langenfeld
authors.forename: A
authors.initials: A
authors.lastname: Friedrich
authors.forename: H P
authors.initials: HP
authors.lastname: Schobel
authors.forename: C D
authors.initials: CD
authors.lastname: Gatzka
authors.forename: H
authors.initials: H
authors.lastname: Weihprecht
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000502:physiology*; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D004032:Diet; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging; D008297:Male; D008875:Middle Aged; D009318:Natriuresis; D012964:Sodium / Q000008:administration & dosage
chemical_list: D000804:Angiotensin II; D012964:Sodium