Aldosterone and corticosterone secretion following midbrain transection

¹ Section on Experimental Cardiovascular Disease, Laboratory of Kidney and Electrolyte Metabolism, National Heart Institute; Section on Endocrinology, National Institute of Arthritis and Metabolic Diseases, Bethesda, Maryland; and Armed Forces Institute of Pathology; and Georgetown University School of Medicine, Washington, D.C.

Following midbrain transection of six normal dogs, secretion rates for aldosterone, corticosterone and Porter-Silber chromogens were not significantly different from values obtained in unoperated dogs; subsequent bleeding increased aldosterone secretion while corticosterone output was unaltered. In five dogs with thoracic caval constriction in which there was a high secretion of aldosterone, midbrain transection was followed by a reduction in inferior vena caval pressure to a level which was apparently too low to sustain the mechanisms resulting in hyperaldosteronism. In one animal aldosterone and corticosterone output was extremely low despite a high venous pressure. In the two dogs with caval constriction in which the venous pressure remained elevated after midbrain transection, the high rate of aldosterone secretion persisted. Bleeding of dogs with caval constriction and midbrain transection resulted in a striking increase in aldosterone secretion. In dogs with caval constriction, corticosterone secretion (5 dogs) and Porter-Silber chromogen output (4 dogs) were high following midbrain transection, and subsequent bleeding failed to increase corticosterone output. It is concluded that complete midbrain transection does not interfere with the high rate of aldosterone secretion which occurs in response to acute blood loss or following caval constriction if venous pressure is maintained at the high control level.

Note:
With the Surgical Assistance of Alfred Casper