Hou Tian-De, Du Ji-Zeng
Division of Physiology, College of Life Sciences, Northwest Normal University, Lanzhou 730070, China.
Acta Pharmacol Sin. 2002 Oct;23(10):878-81.
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.
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.
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).
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.
研究β-内啡肽(β-EP)对清醒大鼠下丘脑正中隆起(ME)和室旁核(PVN)中促甲状腺激素释放激素(TRH)对急性缺氧反应的影响。
采用放射免疫分析法测定脑TRH、血清T3和T4。将雄性Wistar大鼠置于海拔7000米(8.2%氧气)的模拟低压舱中暴露2小时。在缺氧前通过脑室内注射(icv)给予β-EP。
与生理盐水对照组(4.8±0.3)μg/g蛋白质相比,治疗组中β-EP(0.1或1μmol/L,icv)使ME的TRH水平在缺氧期间分别升高12%(P<0.05)和15%(P<0.05),使PVN的TRH分别升高24%(P<0.05)和44%(P<0.01)。同时,血清T3和T4显著降低(P<0.05或P<0.01)。10μmol/L纳洛酮消除了β-EP(0.1μmol/L)对ME(P<0.01)和PVN(P<0.01)中TRH以及T3和T4的影响。单独使用纳洛酮(10μmol/L,icv)降低了ME和PVN中TRH的含量(P<0.05或P<0.01),但提高了血清T3和T4的水平(P<0.01)。
β-内啡肽通过下丘脑ME和PVN中TRH释放的抑制机制参与了大鼠缺氧期间下丘脑TRH释放的调节。