Open AccessAcute Lead Exposure Increases Arterial Pressure: Role of the Renin-Angiotensin System
Author(s) -
Maylla Ronacher Simões,
Rogério Faustino Ribeiro Júnior,
Marcos Vinícius A. Vescovi,
Honério Coutinho de Jesus,
Alessandra Simão Padilha,
Ivanita Stefa,
Dalton Valentim Vassallo,
Mercedes Salaíces,
Mirian Fioresi
Publication year - 2011
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0018730
Subject(s) - blood pressure , medicine , enalapril , losartan , hexamethonium , renin–angiotensin system , mean arterial pressure , endocrinology , angiotensin converting enzyme , cardiology , heart rate , receptor
Background 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. Methodology/Principal Findings 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. Conclusion 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.