Abstract
Mercaptomerin in a dose of 5 mg Hg/kg reduced the renal cortical concentration of hemoglobin. An apparent reduction in medullary hemoglobin levels also occurred. When larger doses (8 to 20 mg Hg/kg) were employed hemoglobin levels in renal cortex continued to decline but concentrations in medulla increased and exceeded control values.
Alterations in concentration or pattern of distribution did not occur during water diuresis.
The dithiol, BAL, could prevent these changes when given immediately following administration of the mercurial but the monothiol, cysteine, could not.
NH4Cl, in doses sufficient to produce an acid urine, prevented the antidiuresis and increase in hemoglobin concentration in rat renal medulla brought about by administration of 8 mg of mercaptomerin Hg/kg. Mercurial depletion of cortical hemoglobin was not affected. Acidifying and alkalinizing salts did not influence renal hemoglobin distribution.
The mercurial compound, p-hydroxymercuri benzoate, which is not diuretic in the normal dog, increased urine flow in the rat. It also depressed renal hemoglobin concentration at a dose of 1 mg Hg/kg. Mercaptomerin was ineffective at this dose level. Chlorothiazide in large doses did not influence hemoglobin concentration in the kidney.
These findings are discussed and an hypothesis regarding potentiation of mercurial diuresis during acidosis is presented.
Footnotes
- Received July 20, 1960.
- © 1961, by The Williams & Wilkins Company
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