Abstract
Conclusions
Pretreatment of unanesthetized or anesthetized dogs with desoxycorticosterone acetate or desoxycorticosterone glycoside did not appreciably affect the diuresis induced by the mercurial mersalyl. In a similar manner ACTH in relatively large doses did not inhibit the mercurial diuresis. Our results indicate that a large dose of mersalyl actually produced a greater effect on tubular sodium reabsorption in the dogs receiving the ACTH. This increased excretion of sodium in the ACTH pretreated dogs is probably due to their initially lower urinary sodium concentration. The average values of the urinary sodium concentration at the time of the mersalyl injection was about 105 ± 12 for the control and 48 ± 6 milliequivalents per liter for the ACTH pretreated dogs. The peak increase in urinary sodium concentration following the mercurial was about 130 ± 4 and 135 ± 6 for the control and ACTH pretreated dogs respectively. It is of interest that the ACTH or DOCA induced reduction in urinary sodium concentration was readily counteracted by mersalyl. Mersalyl probably produced its renal effects by inhibiting some enzyme system essential for sodium reabsorption. Its ability to counteract the adrenocortical effects in the kidney may be due to an action of both these substances on the same enzyme system. However, mersalyl could conceivably produce the same results by acting on a sodium reabsorptive mechanism distal or proximal to the one acted on by the adrenocortical hormones. An action of mercury either distally or proximally could effectively mask the actions of the salt retainingadrenal hormones without necessarily acting directly on the same renal tubular locus affected by the adrenocortical hormones. The results obtained with ACTH are different from those reported by Axelrod and MacLeod(1). Since no details regarding procedures and methods are available at this time, it is not possible to explain the differences in our results and those of Axelrod and MacLeod.
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