Acute effects of thyroid hormones on the production of adrenal cAMP and corticosterone in male rats

Abstract

The acute effects of thyroid hormones on glucocorticoid secretion were studied. Venous blood samples were collected from male rats after they received intravenous 3,5,3′-triiodothyronine (T3) or thyroxine (T4). Zona fasciculata-reticularis (ZFR) cells were treated with adrenocorticotropic hormone (ACTH), T3, T4, ACTH plus T3, or ACTH plus T4 at 37°C for 2 h. Corticosterone concentrations in plasma and cell media, and also adenosine 3′,5′-cyclic monophosphate (cAMP) production in ZFR cells in the presence of 3-isobutyl-1-methylxanthine, were determined. The effects of thyroid hormones on the activities of steroidogenic enzymes of ZFR cells were measured by the amounts of intermediate steroidal products separated by thin-layer chromatography. Administration of T3 and T4 suppressed the basal and the ACTH-stimulated levels of plasma corticosterone. In ZFR cells, both thyroid hormones inhibited ACTH-stimulated corticosterone secretion, but the basal corticosterone was inhibited only with T3>10−10 M or T4>10−8 M. Likewise, T3 or T4 at 10−7 M inhibited the basal- and ACTH-stimulated levels of intracellular cAMP. Physiological doses of T3 and T4 decreased the activities of 3β-hydroxysteroid dehydrogenase, 21-hydroxylase, and 11β-hydroxylase. These results suggest that thyroid hormones counteract ACTH in adrenal steroidogenesis through their inhibition of cAMP production in ZFR cells.

Thyroid Hormone Inhibits Vascular Remodeling Through Suppression of cAMP Response Element Binding Protein Activity

“…In contrast, it was reported that T3 or T4 inhibited basal and corticotropin (ACTH)-stimulated levels of intracellular cAMP in adrenal cells. 21 Incubation with T3 alone did not affect the phosphorylation level of CREB (data not shown) or CRE-dependent gene transcription ( Figure 1B) in our VSMCs. These data may suggest that cAMP level is not affected by T3 in VSMCs and the effect of thyroid hormone on cAMP level may be cell type-dependent.…”

Physiological Roles of Prolactin in the Adrenocortical Response to Acute Restraint Stress

“…One possibility includes a PRLinduced promotion of adrenal steroidogenesis. It is well known that ACTH regulates glucocorticoid secretion through the cyclic AMP (cAMP) pathway [31][32][33][34][35][36][37]. It has been shown that the action of PRL might be mediated through G-protein-adenylate cyclase coupling and cAMP production [38,39], where in chronic hyperprolactinemia enhances receptor-G-protein-adenylate cyclase coupling and cAMP production [2].…”

Direct Effects of Prolactin on Adrenal Steroid Release in Male Hatano High-Avoidance (HAA) Rats May be Mediated Through Janus Kinase 2 (Jak2) Activity

“…Similar effects have been found for PRL o n s e c r e t i o n o f a l d o s t e r o n e , c o r t i s o l , d e h y d r o e p i a n d r o s t e r o n e ( D H E A ) a n d / o r dehydroepiandrosterone sulfate (DHEAS) in human and nonhuman primate adrenals [11, 19- 22]. Moreover, PRL increase in vitro secretion of corticosterone and aldosterone in rat adrenocortical cells [4,[23][24][25][26][27]. In the present study, PRL stimulation of adrenal steroid release was found to be dependent on Jak2 activity since PRL-induced adrenal steroid release was significantly prevented by AG490.…”

“…One possibility is that a PRL induced promotion of adrenal steroidogenesis. It is well known that ACTH regulates glucocorticoid secretion through the cyclic AMP (cAMP) pathway [25,26,[30][31][32][33][34]. Furthermore, adrenal steroidogenic enzymes, including a number of cytochrome P450 family and hydroxysteroid dehydrogenase (HSD) family members, and steroidogenic proteins, such as steroidogenic acute regulatory protein (StAR) and peripheral benzodiazepine binding receptor (PBR), are controlled by ACTH mainly through the cAMP signaling pathway.…”