Sex-Related Interactions of Cadmium and Lead in Changing Cardiovascular Homeostasis and Tissue Metal Levels of Chronically Exposed Rats
The mechanisms by which chronic exposure to lead (Pb), cadmium (Cd) or Pb plus Cd may affect cardiovascular homeostasis are still controversial (Iannaccone et al. 1981; Boscolo et al. 1981; Carmignani et al. 1983). Pb determined sympathetic hyperactivity, baroreflex hyposensitivity, vagal parasympathetic hypofunc-tion, and increased cardiovascular responsiveness to angiotensin II and catecholamines in male Sprague-Dawley rats that received 50 µg/ml of the metal (as acetate) in drinking water for 160–180 days (Iannaccone et al. 1981). Pb also reduced the urinary kallikrein and affected the plasma renin activities of Pb-exposed workers (Boscolo et al. 1978). The mechanisms underlying the cardiac and vascular modifications induced by chronic exposure of both humans and laboratory animals to Cd have been previously reviewed (Carmignani and Boscolo 1984, 1985; Boscolo and Carmignani 1986). Pb and Cd may have additive effects in inducing heart-related diseases or arterial hypertension (Carmignani and Boscolo 1984; Boscolo and Carmignani 1986). However, these additive effects of Pb and Cd were not confirmed in a study carried out on male Sprague-Dawley rats treated with 20 µg/ml of Cd (as acetate) and/or 50 µg/ml of Pb (as acetate) in drinking water for 180-210 days. In this study Cd seemed to act by predominantly peripheral effector mechanisms, while Pb showed central neurogenic actions; both metals altered specifically the levels of zinc (Zn) and copper (Cu) in kidney and brain (Carmignani et al. 1983).
KeywordsPlasma Renin Activity Cardiovascular Responsiveness Cardiovascular Homeostasis Urinary Kallikrein Bilateral Carotid Occlusion
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