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Lead exposure effect on angiotensin II renal vasoconstriction

Department of Molecular Biomedicine, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV); México City, México

Eunice Romo

Department of Molecular Biomedicine, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV); México City, México

Alicia Sanchez-Mendoza

Departament of Pharmacology, Instituto Nacional de Cardiología Ignacio Chávez, México City, México

Amelia Rios

CINVESTAV Monterrey, Monterry, Mexico

Virgilia Soto

Department of Pathology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico

M. Carmen Avila-Casado

Department of Pathology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico

Armando Medina

Department of Pathology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico

Bruno Escalante

Department of Molecular Biomedicine, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV); México City, México, bescalan{at}cinvestav.mx, CINVESTAV Monterrey, Monterry, Mexico

Low levels of chronic lead exposure can produce hypertension and endothelial dysfunction, which could be associated with oxidative stress, changes in vascular tone and an imbalance of endothelial-derived vasoconstriction and vasodilator factors. The aim was to investigate the effect of chronic lead-exposure on angiotensin II-induced vasoconstriction in isolated perfused kidney and microvessels. Male Wistar rats (230—250 g) were treated for 12 weeks with lead acetate (100 ppm, Pbgroup) or pure water (control group). We evaluated the vascular reactivity in the kidneys and renal microvessels in the presence and absence of N-nitro-L-arginine methyl ester (L-NAME) in both groups. The nitrite concentration in renal perfusate was measured as an index of NO released, renal abundance of 3-nitrotyrosine was measured as well as endothelial NO synthase (eNOS) expression. Oxidative stress was measured by using the oxidative fluorescence dye dihydroethidium (DHE) to evaluate in situ production of superoxide and identified by confocal microscopy. Lead-exposure significantly increased blood pressure, eNOS protein expression, oxidative stress and vascular reactivity to angiotensin II. L-NAME potentiated vascular response to angiotensin II in control group but had no effect on the Pb-group. Nitrites released from the kidney of lead-group was lower compared to the control group while 3-nitrotyrosine was higher. This data suggest that lead-induced hypertension could be caused partially by an altered NOsystem. Human & Experimental Toxicology (2007) 26: 499—507

Human & Experimental Toxicology, Vol. 26, No. 6, 499-507 (2007)
DOI: 10.1177/0960327106077597


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