Blocking of central nervous mineralocorticoid receptors counteracts inhibition of pituitary-adrenal activity in human sleep
Blocking of central nervous mineralocorticoid receptors counteracts inhibition of pituitary-adrenal activity in human sleep
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DOI：
10.1210/jc.82.4.1106
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发表时间：
1997-04-01
影响因子：
5.8
通讯作者：
Fehm, HL
中科院分区：
文献类型：
--
作者：
Born, J;Steinbach, D;Fehm, HL
研究发现，人类夜间睡眠早期的垂体-肾上腺活性受到抑制。这种抑制作用被认为反映了以盐皮质激素受体（MR）表达为特征的海马细胞的调节影响。在 9 名健康男性中，每人在 4 次检查中，每人对 CRH（50 μg）推注的垂体肾上腺反应性：在夜间早期睡眠期间或在受试者保持清醒的夜间同一时间注射 CRH。这两种条件均在用选择性 MR 拮抗剂 Canrenoate 预处理（2 x 200 mg，0800 和 1700 小时，实验当晚之前）和安慰剂给药后进行。服用安慰剂后，睡眠使 CRH 的 ACTH 和皮质醇分泌反应减少至清醒时观察到的约 65%（P < 0.05）。在坎雷诺酸治疗后，睡眠和清醒期间的 ACTH 和皮质醇分泌反应没有差异，并且与安慰剂治疗受试者在清醒期间获得的反应相当。与安慰剂相比，canrenoate 还明显减少了慢波睡眠时间（P < 0.005）。研究结果证实了早期睡眠期间垂体-肾上腺反应性受到抑制。 MR 阻断后抑制消失表明睡眠通过中枢神经 MR 表达细胞发挥这种影响。这些细胞似乎同时参与慢波睡眠的产生。
Pituitary-adrenal activity has been found to be inhibited during early nocturnal sleep in humans. This inhibition was supposed to reflect a regulatory influence of hippocampal cells characterized by the expression of mineralocorticoid receptors (MR). Pituitary adrenal responsiveness to bolus injections of CRH (50 mu g) was examined in each of nine healthy men on four occasions: CRH was injected either during early nocturnal sleep or at the same time of night while the subject was kept awake. Both of these conditions were run after pretreatment with the selective MR antagonist, canrenoate (2 x 200 mg, 0800 and 1700 h, preceding the experimental night) and after placebo administration. After placebo, sleep reduced ACTH and cortisol secretory responses to CRH to about 65% of the size observed during wakefulness (P < 0.05). After canrenoate, ACTH and cortisol secretory responses during sleep and wakefulness did not differ and were comparable with those obtained in placebo-treated subjects during wakefulness. Compared with placebo, canrenoate also distinctly reduced the time spent in slow-wave sleep (P < 0.005). The findings confirm an inhibition of pituitary-adrenal responsiveness during early sleep. The inhibition disappearance after blockage of MR suggests that sleep exerts this influence via central nervous MR-expressing cells. These cells seem to be simultaneously involved in the generation of slow-wave sleep.