Rats were exposed for 10 months to 60 ppm of Pb (as acetate) in drinking water. Systolic and diastolic blood pressure and cardiac inotropism were increased by the metal, which reduced arterial blood flow and unaffected heart rate. The activities of plasma angiotensin I-converting enzyme (ACE) and kininase II were strongly augmented by Pb, suggesting markedly increased and decreased levels of plasma angiotensin II and bradykinin, respectively. Moreover, the Pb-exposed rats showed a lower increase of the plasma kallikrein and kininase I activities. These results are discussed in the context of the complex relationships linking the renin-angiotensin-aldosterone (RAA), kallikrein-kinin and other autacoidal, neurohumoral (e.g., catecholaminergic) and transductional systems (e.g., nitric oxide (NO)). Pb was confirmed to induce arterial hypertension and cardiovascular alterations at plasma levels similar to those observed in the general population or in subjects with short occupational exposure.