RESUMO
Chronic exposure to low levels of lead results in sustained hypertension in humans and experimental animals. The mechanism of lead-induced hypertension remains unclear. We investigated the short-term (4 and 8 weeks) and subchronic (12 weeks) effects of lead treatment on responsiveness of vascular adrenergic system and level of nitric oxide metabolites, that is, total nitrates and nitrites (NOx). Male Sprague-Dawley rats were treated with lead acetate (100 ppm in drinking water) for 12 weeks. Short-term lead administration resulted in marked elevation of blood pressure accompanied by significant reduction in serum NOx levels. In contrast, after subchronic lead administration the trend of decrease in NOx levels somehow reversed despite further increase in blood pressure. Both short-term and subchronic lead administration resulted in significant differences in vascular reactivity with respect to either vasoconstrictor (phenylephrine and clonidine) or vasodilator (isoproterenol) agents. We conclude that vascular adrenergic system and nitric oxide pathway change in short-term and subchronic phases of lead poisoning.