Acute effects of lead on renal electrolyte excretion and plasma renin activity

Abstract

Since lead accumulates in the kidney and interferes with the renal transport of amino acids and glucose, we tested the hypothesis that acute doses of lead also reduce tubular electrolyte reabsorption and alter the secretion of renin. In sodium pentobarbital-anesthetized dogs, acute iv lead increased the excretion of sodium, potassium, calcium, and water, despite a constant glomerular filtration rate; therefore lead reduced the tubular reabsorption of these substances. Lead also caused an increase in plasma renin activity. The threshold dose of acutely administered lead necessary to elicit these responses was determined in dose-response experiments on unanesthetized rats; a dose of 0.1 mg of lead/kg was sufficient to cause significant increases in plasma renin and the renal excretion of sodium. Lead concentrations in the tissues of the rats were measured in samples taken immediately at the conclusion of the study; the threshold dose of lead was associated with very low blood lead (< 5 [mu]g/100 ml) and kidney lead (1.2 [mu]g/g wet wt). These effects of lead are discussed with regard to their possible clinical significance.