title: Acute lead exposure increases arterial pressure: role of the renin-angiotensin system.
abstract: Chronic lead exposure causes hypertension and cardiovascular disease. Our purpose was to evaluate the effects of acute exposure to lead on arterial pressure and elucidate the early mechanisms involved in the development of lead-induced hypertension.
  
  
  
  Wistar rats were treated with lead acetate (i.v. bolus dose of 320 µg/Kg), and systolic arterial pressure, diastolic arterial pressure and heart rate were measured during 120 min. An increase in arterial pressure was found, and potential roles of the renin-angiotensin system, Na(+),K(+)-ATPase and the autonomic reflexes in this change in the increase of arterial pressure found were evaluated. In anesthetized rats, lead exposure: 1) produced blood lead levels of 37±1.7 µg/dL, which is below the reference blood concentration (60 µg/dL); 2) increased systolic arterial pressure (Ct: 109±3 mmHg vs Pb: 120±4 mmHg); 3) increased ACE activity (27% compared to Ct) and Na(+),K(+)-ATPase activity (125% compared to Ct); and 4) did not change the protein expression of the α1-subunit of Na(+),K(+)-ATPase, AT(1) and AT(2). Pre-treatment with an AT(1) receptor blocker (losartan, 10 mg/Kg) or an ACE inhibitor (enalapril, 5 mg/Kg) blocked the lead-induced increase of arterial pressure. However, a ganglionic blockade (hexamethonium, 20 mg/Kg) did not prevent lead's hypertensive effect.
  
  
  
  Acute exposure to lead below the reference blood concentration increases systolic arterial pressure by increasing angiotensin II levels due to ACE activation. These findings offer further evidence that acute exposure to lead can trigger early mechanisms of hypertension development and might be an environmental risk factor for cardiovascular disease.
authors.affiliation: Physiological Sciences Post-Graduation Program, Federal University of Espírito Santo, Vitoria, Espírito Santo, Brazil.
authors.forename: Maylla Ronacher
authors.initials: MR
authors.lastname: Simões
authors.forename: Eduardo Hertel
authors.initials: EH
authors.lastname: Ribeiro
authors.forename: Marcos Vinícius A
authors.initials: MV
authors.lastname: Vescovi
authors.forename: Honério C
authors.initials: HC
authors.lastname: de Jesus
authors.forename: Alessandra S
authors.initials: AS
authors.lastname: Padilha
authors.forename: Ivanita
authors.initials: I
authors.lastname: Stefanon
authors.forename: Dalton V
authors.initials: DV
authors.lastname: Vassallo
authors.forename: Mercedes
authors.initials: M
authors.lastname: Salaices
authors.forename: Mirian
authors.initials: M
authors.lastname: Fioresi
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects* / Q000502:physiology / Q000503:physiopathology; D001341:Autonomic Nervous System / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D004781:Environmental Exposure; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology; D007854:Lead / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012018:Reflex / Q000502:physiology; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
chemical_list: D007854:Lead; D007703:Peptidyl-Dipeptidase A; D000254:Sodium-Potassium-Exchanging ATPase