Premium
ADRENOCORTICOID‐DEPENDENT α‐LACTALBUMIN SYNTHESIS IN RAT MAMMARY GLAND EXPLANTS: ANTAGONIST STUDIES
Author(s) -
Quirk Susan J.,
Gannell Jennifer E.,
Funder John W.
Publication year - 1986
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1986.tb00341.x
Subject(s) - endocrinology , medicine , corticosterone , mineralocorticoid , mineralocorticoid receptor , aldosterone , glucocorticoid , glucocorticoid receptor , agonist , antagonist , adrenal gland , chemistry , receptor , biology , hormone
SUMMARY 1. Though adrenal steroids are required for the production of α‐lactalbumin by mammary gland explants, the physiological class of steroid activity (mineralocorticoid, glucocorticoid) remains to be established. 2. α‐Lactalbumin production by mammary gland explants from mid‐pregnant rats has been shown in previous studies to be increased by high doses of aldosterone, but not by deoxycorticosterone; in six of 11 experiments corticosterone, the physiological glucocorticoid in the rat, elevated α‐lactalbumin; in five other studies corticosterone had no effect. 3. In the present studies the mineralocorticoid antagonist, spirolactone, at very high doses (3‐10 μmol/1) blocked the stimulatory effect on α‐lactalbumin levels of both 30 nmol/1 corticosterone and 3 nmol/1 RU 26988, a pure synthetic glucocorticoid (Type II) receptor agonist. 4. Receptor studies, however, indicated that this antagonism is consistent with Type II, glucocorticoid receptor occupancy by spirolactone. 5. Since deoxycorticosterone is without agonist effect, and only very high doses of spirolactone affect α‐lactalbumin synthesis, we conclude that the effect of adrenal steroids on α‐lactalbumin production is a manifestation of glucocorticoid and not mineralocorticoid activity.