Abstract
Prolonged exposure to low levels of lead causes systemic hypertension. Several mechanisms have been proposed to explain lead-induced hypertension. Recently, the etiological role of the renin–angiotensin system (RAS) has been investigated in this context. This study assessed the alterations of circulatory and tissue angiotensin converting enzyme (ACE) activity during development of lead induced hypertension. Male rats were divided to two main groups: lead-treated animals which received lead acetate, 100 ppm, in drinking water for 2, 4, 6, and 8 weeks and a control group given distilled water. The ACE activity in serum and tissues was analyzed by HPLC. The blood pressure gradually increased in correlation with lead exposure with time. The study also revealed significant elevation of local and serum ACE activity in the early phase of lead treatment; however, chronic lead exposure suppressed ACE activity in serum and tissues. These results emphasize the etiological role of ACE activity in the early phase of lead-induced hypertension.
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