Abstract
Endocrine factors different from ACTH or angiotensin II can stimulate aldosterone
secretion and have a role in the pathophysiology of hyperaldosteronism. Aldosterone
may increase in luteotropic/progestogenic and in hypothyroid states; LH and, occasionally,
TSH receptors have been detected in normal adrenal cortex and aldosterone-producing
adenoma. The aim of the study was to compare adrenal contents of LH and TSH receptors
between normal cortex and aldosterone-producing adenoma and to evaluate the ability
of LH, its product progesterone, and TSH to stimulate aldosterone secretion in vitro
from primary adrenocortical cells. Surgical aldosterone-producing adenoma fragments
from 19 patients and adrenal cortex fragments from 10 kidney donors were used for
Western blotting and cell cultures. LH (n=26), TSH (n=19) and progesterone (n=8) receptor
proteins were investigated; LH receptor-mRNA was also tested in 8 samples. Aldosterone
responses in vitro to LH, progesterone, and TSH stimulation were assayed. LH and TSH
receptors were more expressed in adenoma than normal cortex (p<0.01, p<0.05, respectively);
progesterone receptor was observed in 6/8 samples. Aldosterone increased after in
vitro stimulation with LH (5/12 adenoma, 1/7 normal cells), progesterone (4/5 adenoma,
5/6 normal cells), and TSH (3/5 adenoma and 3/5 normal cells). LH and TSH receptors
were more expressed in aldosterone producing adenoma than normal adrenal cortex. LH,
progesterone, and TSH can stimulate aldosterone in vitro. Similar mechanisms could
participate in vivo in the aldosterone increase in lutheotropic, progestogenic, or
hypothyroid states and may exist in both normal adrenal cortex and adenoma in responsive
individuals.
Key words
LH receptor - TSH receptor - progesterone - aldosterone
