| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
The Second Department of Internal Medicine Hokkaido University School of Medicine, Sapporo, Japan
Insulin-induced hypoglycemia caused an increase in plasma aldosterone as well as in renin activity and cortisol. After the suppression of the renin-angiotensin system by the prior administration ol propranolol, insulin-induced hypoglycemia still caused a significant increase in plasma aldosterone similar to the increase in plasma cortisol, though plasma renin activity was suppressed. Conversely, after the suppression of endogenous ACTH by the prior administration of dexamethasone, insulin-induced hypoglycemia failed to induce a rise in plasma aldosterone and plasma cortisol, though plasma renin activity increased. The increase of plasma aldosterone in response to exogenous ACTH was not different with or without the prior administration of dexamethasone.
We conclude that ACTH is largely responsible for the increased aldosterone secretion after insulininduced hypoglycemia.
* Present Address: The Department of Biochemistry, Higashi Nippon Cakuen University School of Pharmacy, Tobetsu, Japan.
Received December 1, 1975.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |