title: Sympathetic and renin-angiotensin systems contribute to increased blood pressure in sucrose-fed rats.
abstract: BACKGROUND
  This study evaluated the effect of chronic sucrose feeding on hemodynamic parameters and renal sympathetic nervous activity. In addition, angiotensin I, II, and 1-7 levels were determined in plasma, heart, kidney, and the epididymal adipose tissue.
  
  
  METHODS
  Male Wistar rats were treated for 30 days with 20% sucrose solution (n = 21) or tap water (n = 19) and food ad libitum. Blood pressure, cardiac output, and total peripheral resistance were recorded at the end of the 30-day treatment period. Sympathetic and angiotensinergic systems were evaluated by acute hexamethonium and captopril administration; plasma and tissue (heart, kidney, and epididymal adipose tissue) angiotensins were measured by high-performance liquid chromatography; and angiotensin-converting enzyme activity was determined by continuous fluorescent assay. Plasma renin activity and plasma levels of insulin and leptin were evaluated by radioimmunoassay.
  
  
  RESULTS
  Chronic sucrose feeding was associated with increased blood pressure (BP) (129 +/- 1 v 102 +/- 3 mm Hg) and circulating insulin (171%) and leptin (356%) levels when compared with the control group. The sucrose group also showed a 27% higher renal sympathetic nervous activity. The depressor response to hexamethonium was similar in both groups, whereas captopril caused a more pronounced decrease in BP in the sucrose group than in controls (-40 +/- 2 v -11 +/- 2 mm Hg), possibly reflecting the higher plasma renin activity and plasma content of angiotensin II and renal angiotensin II in sucrose rats.
  
  
  CONCLUSIONS
  These findings suggest a specific renal renin-angiotensin-sympathetic activation as a potential mechanism for the cardiovascular changes in response to chronic sucrose feeding.
authors.affiliation: Department of Physiology, Universidade Federal de São Paulo, São Paulo, Brazil.
authors.forename: Raphael R de A
authors.initials: RR
authors.lastname: Freitas
authors.forename: Karen L
authors.initials: KL
authors.lastname: Lopes
authors.forename: Bruno A
authors.initials: BA
authors.lastname: Carillo
authors.forename: Cassia T
authors.initials: CT
authors.lastname: Bergamaschi
authors.forename: Adriana K
authors.initials: AK
authors.lastname: Carmona
authors.forename: Dulce E
authors.initials: DE
authors.lastname: Casarini
authors.forename: Luzia
authors.initials: L
authors.lastname: Furukawa
authors.forename: Joel C
authors.initials: JC
authors.lastname: Heimann
authors.forename: Ruy R
authors.initials: RR
authors.lastname: Campos
authors.forename: Miriam S
authors.initials: MS
authors.lastname: Dolnikoff
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000809:Angiotensins / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D002216:Captopril / Q000494:pharmacology; D002302:Cardiac Output / Q000502:physiology; D019422:Dietary Sucrose / Q000009:adverse effects*; D018738:Hexamethonium / Q000494:pharmacology; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D007668:Kidney / Q000187:drug effects / Q000502:physiology; D020738:Leptin / Q000097:blood; D008297:Male; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology*; D012964:Sodium / Q000097:blood / Q000652:urine; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000809:Angiotensins; D019422:Dietary Sucrose; D007328:Insulin; D020738:Leptin; D018738:Hexamethonium; D002216:Captopril; D012964:Sodium; D012083:Renin