title: Norepinephrine attenuates hypoxia-inhibited thyrotropin-releasing hormone release in median eminence and paraventricular nucleus of rat hypothalamus.
abstract: OBJECTIVE
  We have previously found that chronic hypoxia inhibited thyrotropin-releasing hormone (TRH) mRNA expression in rat paraventricular nucleus (PVN). This study presented the effects of hypoxia on TRH secretion in rat hypothalamus, and the norepinephrine (NE) involvement in the modulation of TRH secretion during acute hypoxia exposure.
  
  
  METHODS
  Hypoxia was simulated at altitudes of 5 km (10.8% O2) or 7 km (8.2% O2) in a ventilated hypobaric chamber, and control group was set at local altitude of 2.3 km (15.8% O2). The duration of hypoxia exposure was designed acutely and chronically for 0.5, 2, 24 h, 5, 10, and 30 d, respectively. TRH levels were measured by specific radioimmunoassay.
  
  
  RESULTS
  The results showed that hypoxia of 5 km or 7 km significantly enhanced TRH levels of the ME and PVN, and reduced serum T3 levels in most hypoxia-exposed groups. Intraventricular injection (icv) of NE (4 nmol/L) induced a decrease in TRH levels in the median eminence (ME) and PVN, and an increased serum T3 levels following hypoxia of 7 km exposure for 2 h, compared with icv saline control, indicating TRH release increased. The stimulating effect of NE on the TRH secretion was abolished by icv antagonist of adrenergic alpha2-receptor, yohimbine (40 nmol/L).
  
  
  CONCLUSIONS
  We conclude that acute and chronic hypoxia exposure produces an inhibition of hypothalamic TRH secretion from the ME and PVN. Central adrenergic system may play a stimulating role through alpha2-receptor in the acute hypoxia-modulating TRH release from rat hypothalamus.
authors.affiliation: Physiology Group, College of Life Sciences, Northwest Normal University, Lanzhou 730070, China.
authors.forename: Tian-De
authors.initials: TD
authors.lastname: Hou
authors.forename: Ji-Zeng
authors.initials: JZ
authors.lastname: Du
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000317:Adrenergic alpha-Antagonists / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D001273:Atmosphere Exposure Chambers; D001274:Atmospheric Pressure; D000860:Hypoxia / Q000188:drug therapy* / Q000503:physiopathology*; D007276:Injections, Intraventricular; D008297:Male; D008473:Median Eminence / Q000187:drug effects / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology*; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000378:metabolism*; D011863:Radioimmunoassay; D051381:Rats; D017208:Rats, Wistar; D018341:Receptors, Adrenergic, alpha-2 / Q000187:drug effects; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism*; D014284:Triiodothyronine / Q000378:metabolism; D015016:Yohimbine / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D018341:Receptors, Adrenergic, alpha-2; D014284:Triiodothyronine; D015016:Yohimbine; D013973:Thyrotropin-Releasing Hormone; D009638:Norepinephrine