Terminal progress report: lead - its renal handling, renin, and erythropoietin.
University of Michigan, Ann Arbor Michigan 1983 Jan; :1-3
The purposes of the project were to determine whether chronic lead (7439921) exposure caused permanent changes in the renin/angiotensin system and to investigate the mechanisms for handling of leaf and other trace metals, especially zinc (7440666), by the kidney. The offspring of pregnant, lactating rats when both were exposed to 100 micrograms per milliliter lead in their drinking water developed hypertension that persisted for 6 months. The hypertension was associated with low plasma concentrations of renin and angiotensin, strongly indicating that the hypertension was not due to hyperactivity of the renin/angiotensin system. Lower doses of lead, 5 and 25 parts per million (ppm), did not induce hypertension, but caused dose dependent elevations of plasma renin. Additional experiments in lead exposed, non hypertensive rats and rabbits indicated that renin secretion was the cause of increased plasma renin. Chronic treatment of dogs and rats with up to 500ppm lead inhibited tubular reabsorption of zinc, resulting in increased urinary excretion of zinc. This was associated with significant decreases in plasma zinc concentrations.
NIOSH-Grant; Trace-metals; Renal-absorption; Hormone-activity; Lead-fumes; Excretion; Trace-metals; Animal-studies; Exposure-methods; Enzymes
Final Grant Report
Other Occupational Concerns; Grants-other
University of Michigan, Ann Arbor Michigan
University of Michigan at Ann Arbor, Ann Arbor, Michigan