title: During a corticotropin-releasing hormone test in healthy subjects, administration of a beta-adrenergic antagonist induced secretion of cortisol and dehydroepiandrosterone sulfate and inhibited secretion of ACTH.
abstract: OBJECTIVE
  In chronic inflammatory diseases, serum levels of dehydroepiandrosterone (DHEA) sulfate (DHEAS) are low. Interestingly, several non-inflammatory diseases display similarly low levels of DHEAS which points to other inhibitory factors such as an activated sympathetic nervous system (SNS) (e.g. in patients with heart failure, fibromyalgia, or cancer cachexia). We aimed to identify the influence of the SNS tone on stimulated adrenal steroid secretion in 16 male and 12 female healthy subjects.
  
  
  METHODS
  One group were given oral propranolol 2 h before a corticotropin-releasing hormone (CRH) test, and levels of adrenocorticotropin (ACTH), cortisol, 17-hydroxyprogesterone (17OHP), androstenedione, DHEA, and DHEAS were measured.
  
  
  RESULTS
  Propranolol treatment decreased heart rate (by 20%), diastolic blood pressure (by 20%), and plasma ACTH, and increased serum cortisol, serum DHEAS, and the molar ratio of cortisol/17OHP, cortisol/DHEA, and DHEAS/DHEA similarly in female and male subjects.
  
  
  CONCLUSIONS
  A beta-adrenergic influence seems to decrease CRH-stimulated cortisol in relation to ACTH and 17OHP, and decreases DHEAS in relation to DHEA. Although other workers have found beta-adrenergic stimulation of steroid secretion in cultured adrenocortical cells, the overall systemic influence of the SNS via beta-adrenoceptors seems to inhibit adrenal steroids under unstimulated and stimulated conditions. Sympathetic hyperactivity may be a common denominator for low levels of DHEAS in inflammatory and non-inflammatory diseases.
authors.affiliation: Department of Internal Medicine I, University Hospital of Regensburg, 93042 Regensburg, Germany.
authors.forename: Selda
authors.initials: S
authors.lastname: Kizildere
authors.forename: Thomas
authors.initials: T
authors.lastname: Glück
authors.forename: Bettina
authors.initials: B
authors.lastname: Zietz
authors.forename: Jürgen
authors.initials: J
authors.lastname: Schölmerich
authors.forename: Rainer H
authors.initials: RH
authors.lastname: Straub
mesh_terms: D015067:17-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D019326:17-alpha-Hydroxyprogesterone / Q000097:blood; D000311:Adrenal Glands / Q000201:enzymology; D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage*; D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism*; D000328:Adult; D000735:Androstenedione / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism; D003687:Dehydroepiandrosterone / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood / Q000378:metabolism*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism*; D008297:Male; D011433:Propranolol / Q000008:administration & dosage*; D012737:Sex Factors; D013254:Steroid 17-alpha-Hydroxylase / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000187:drug effects
chemical_list: D000319:Adrenergic beta-Antagonists; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D019326:17-alpha-Hydroxyprogesterone; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D011433:Propranolol; D015067:17-Hydroxysteroid Dehydrogenases; C044256:3 (or 17)-beta-hydroxysteroid dehydrogenase; D013254:Steroid 17-alpha-Hydroxylase; D006854:Hydrocortisone