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.
1 The aim of this study was to investigate the mechanism by which amphetamine exerts its inhibitory e ect on testicular interstitial cells of male rats. 2 Administration of amphetamine (10 712 ± 10 76 M) in vitro resulted in a dose-dependent inhibition of both basal and human chorionic gonadotropin (hCG, 0.05 iu ml 71 )-stimulated release of testosterone. 3 Amphetamine (10 79 M) enhanced the basal and hCG-increased levels of adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation in vitro (P50.05) in rat testicular interstitial cells. 4 Administration of SQ22536, an adenylyl cyclase inhibitor, decreased the basal release (P50.05) of testosterone in vitro and abolished the inhibitory e ect of amphetamine. 5 Nifedipine (10 76 M) alone decreased the secretion of testosterone (P50.01) but it failed to modify the inhibitory action of amphetamine (10 710 ± 10 76 M). 6 Amphetamine (10 710 ± 10 76 M) signi®cantly (P50.05 or P50.01) decreased the activities of 3b-hydroxysteroid dehydrogenase (3b-HSD), P450c17, and 17-ketosteroid reductase (17-KSR) as indicated by thin-layer chromatography (t.l.c.). 7 These results suggest that increased cyclic AMP production, decreased Ca 2+ channel activity and decreased activities of 3b-HSD, P450c17, and 17-KSR are involved in the inhibition of testosterone production induced by the administration of amphetamine.
1 The e ect of amphetamine on gastrointestinal (GI) transit and the plasma levels of cholecystokinin (CCK) were studied in male rats. 2 Gastric emptying was inhibited both acutely and chronically by the administration of amphetamine. GI transit was decreased by the acute administration of amphetamine but not a ected by the chronic administration of amphetamine. 3 Plasma CCK levels were increased dose-dependently by amphetamine. 4 Proglumide, a CCK receptor antagonist, prevented amphetamine-induced inhibition of gastric emptying and the decrease in GI transit in male rats. 5 The selective CCK A receptor antagonist, lorglumide, dose-dependently attenuated the amphetamineinduced inhibition of gastric emptying in male rats. In contrast, the selective CCK B receptor antagonist, PD 135,158, did not reverse the e ect of amphetamine on gastric emptying. 6 Both lorglumide and PD 135,158 reversed the inhibitory e ect of amphetamine on GI transit in male rats. 7 These results suggest that amphetamine-induced inhibition of gastric emptying and intestinal transit is due in part to a mechanism associated with the hypersecretion of endogenous CCK.
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