title: Relationships between left ventricular mass and the renin-angiotensin system, catecholamines, insulin and leptin.
abstract: OBJECTIVE
  Several neurohormonal systems have been suggested to stimulate myocardial cell growth, and thus take part in the development of left ventricular (LV) hypertrophy. We studied associations between LV mass and markers of the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system, glucose homeostasis and leptin.
  
  
  METHODS
  A total of 115 hypertensive patients with LV hypertrophy and two age- and gender-matched control groups consisting of 38 hypertensive patients without LV hypertrophy and 38 normotensive subjects were included. We examined determinants of the RAAS, plasma levels and 24-h urinary excretions of noradrenaline and adrenaline, plasma proinsulin, insulin, glucose, leptin and LV mass by echocardiography.
  
  
  RESULTS
  Plasma renin activity (PRA) and serum aldosterone were higher (both P < 0.001) in the LV hypertrophy group than in patients without LV hypertrophy and normotensive subjects (1.0 +/- 0.8, 0.2 +/- 0.2 and 0.2 +/- 0.2 ng mL(-1) h(-1), and 327 +/- 126, 269 +/- 146 and 221 +/- 80 pmol L(-1), respectively). PRA and aldosterone both related (P < 0.001) to LV mass index (r = 0.44 and 0.27, respectively). Catecholamine levels and excretions were similar in all three groups and did not relate to LV mass index. Proinsulin, insulin and leptin levels were all elevated in the hypertensive patients (P < 0.01), but proinsulin, insulin, insulin sensitivity (by the homeostasis model assessment) and leptin did not relate to LV geometry, when indexed for body size.
  
  
  CONCLUSIONS
  Plasma renin activity and serum aldosterone levels are elevated in hypertensive LV hypertrophy and relate to LV mass index. In addition to blood pressure, activation of the RAAS may be an important nonhaemodynamic mechanism in the control of LV hypertrophy.
authors.affiliation: Division of Internal Medicine, Karolinska Institutet Danderyd Hospital, Stockholm, Sweden. karin.malmqvist@med.ds.sll.se
authors.forename: K
authors.initials: K
authors.lastname: Malmqvist
authors.forename: K P
authors.initials: KP
authors.lastname: Ohman
authors.forename: L
authors.initials: L
authors.lastname: Lind
authors.forename: F
authors.initials: F
authors.lastname: Nyström
authors.forename: T
authors.initials: T
authors.lastname: Kahan
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure / Q000502:physiology; D002395:Catecholamines / Q000097:blood*; D004452:Echocardiography / Q000379:methods; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000097:blood; D017379:Hypertrophy, Left Ventricular / Q000097:blood*; D007328:Insulin / Q000097:blood*; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012084:Renin-Angiotensin System / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D002395:Catecholamines; D007328:Insulin; D020738:Leptin