Beta-endorphin suppresses release of thyrotropin-releasing hormone in rat hypothalamus during acute hypoxia exposure.
Abstract
AIM: To study the influences of beta-endorphin (beta-EP) on the responses of
thyrotropin-releasing hormone (TRH) in median eminence (ME) and paraventricular
nucleus (PVN) of hypothalamus to acute hypoxia in conscious rats.
METHODS: Brain TRH, serum T3 and T4 were measured by radioimmunoassay. The male
Wistar rats were exposed in a simulated hypobaric chamber at 7000 m altitude (8.2
% O2) for 2 h. beta-EP was given by intraventricular injection (icv) before
hypoxia.
RESULTS: beta-EP (0.1 or 1 micromol/L, icv) elevated TRH levels of ME by 12 % (P
<0.05) and 15 % (P < 0.05) in treated groups comparing with saline control group
(4.8+/-0.3) microg/g protein, and enhanced TRH of PVN by 24 % (P <0.05) and 44 %
(P < 0.01) in treated groups comparing with control group (180+/-21) ng/g protein
during hypoxia. Meanwhile, serum T3 and T4 were significantly decreased (P < 0.05
or P < 0.01). Naloxone 10 micromol/L abolished the effects of beta-EP (0.1
micromol/L) on TRH in ME (P <0.01) and PVN (P < 0.01) as well as T3 and T4.
Naloxone (10 micromol/L, icv) alone reduced contents of TRH in ME and PVN (P
<0.05 or P <0.01), but increased the levels of serum T3 and T4 (P <0.01).
CONCLUSION: beta-Endorphin was involved in the modulation of hypothalamic TRH
release of rats during hypoxia, through an inhibitory mechanism of TRH release in
ME and PVN of hypothalamus.
Keywords:
thyrotropin-releasing hormone (TRH) in median eminence (ME) and paraventricular
nucleus (PVN) of hypothalamus to acute hypoxia in conscious rats.
METHODS: Brain TRH, serum T3 and T4 were measured by radioimmunoassay. The male
Wistar rats were exposed in a simulated hypobaric chamber at 7000 m altitude (8.2
% O2) for 2 h. beta-EP was given by intraventricular injection (icv) before
hypoxia.
RESULTS: beta-EP (0.1 or 1 micromol/L, icv) elevated TRH levels of ME by 12 % (P
<0.05) and 15 % (P < 0.05) in treated groups comparing with saline control group
(4.8+/-0.3) microg/g protein, and enhanced TRH of PVN by 24 % (P <0.05) and 44 %
(P < 0.01) in treated groups comparing with control group (180+/-21) ng/g protein
during hypoxia. Meanwhile, serum T3 and T4 were significantly decreased (P < 0.05
or P < 0.01). Naloxone 10 micromol/L abolished the effects of beta-EP (0.1
micromol/L) on TRH in ME (P <0.01) and PVN (P < 0.01) as well as T3 and T4.
Naloxone (10 micromol/L, icv) alone reduced contents of TRH in ME and PVN (P
<0.05 or P <0.01), but increased the levels of serum T3 and T4 (P <0.01).
CONCLUSION: beta-Endorphin was involved in the modulation of hypothalamic TRH
release of rats during hypoxia, through an inhibitory mechanism of TRH release in
ME and PVN of hypothalamus.