Abstract

The effect of BAL on the renal concentration and urinary excretion of mercury was examined in acute experiments in the dog. Following the administration of mercuric cysteine, BAL-induced mercury excretion was pH dependent, increasing in an alkaline urine, and remaining unchanged with an acid urine. However, the loss of mercury from the renal parenchyma did not vary with urinary pH. With an alkaline urine, the renal decrement can be attributed to urinary excretion; with an acid urine, mercury is lost from the kidney largely to become redistributed within the body.

Following the administration of chiormerodrin cysteine, BAL increased the urinary excretion of mercury, an effect that was independent of urinary pH.

Following mersalyl cysteine, BAL had little effect on the rate of urinary mercury excretion.

The degree of diuresis appears unrelated to the amount of total mercury in the renal parenchyma. This phenomenon is discussed particularly in relationship to mersalyl cysteine. The findings suggest that diuresis is a consequence of the action on a specific renal receptor by a very small amount of mercury.