Adrenergic beta(1)- and beta(1+2)-receptor blockade suppress the natural killer cell response to head-up tilt in humans
Adrenergic beta(1)- and beta(1+2)-receptor blockade suppress the natural killer cell response to head-up tilt in humans
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DOI：
10.1152/jappl.1997.83.5.1492
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发表时间：
1997-11-01
影响因子：
3.3
通讯作者：
Pedersen, BK
中科院分区：
文献类型：
--
作者：
Klokker, M;Secher, NH;Pedersen, BK
为了评估应激引起的血白细胞变化，重点是自然杀伤(NK)细胞，对8名男性志愿者进行了三次直立倾斜试验，分别使用肾上腺素能β(1)-(美托洛尔)和β(1+2)-(心得安)阻滞剂和生理盐水(对照组)。阻断β(1)和β(1+2)受体不影响突触前症状的出现，但直立倾斜引起的一过性淋巴细胞增多可被β(1+2)受体阻断而不能被β1受体阻断所消除。头朝上倾斜还会导致迟发性中性粒细胞增多，对β受体阻滞剂不敏感。淋巴细胞亚群分析显示，直立倾斜可使外周血中CD3(-)/CD16(+)和CD3(-)/CD56(+)NK细胞的百分率和绝对数增加一倍，美托洛尔可部分阻断这一增加，而心得安则可阻断这一增加。在直立倾斜过程中，每个NK细胞的NK细胞活性没有变化，这表明招募到循环中的NK细胞的细胞毒能力没有变化。这些数据表明，直立倾斜诱导的淋巴细胞增多主要是由于CD16(+)和CD56(+)NK细胞，它们向血液中的募集被β1，尤其是β(1+2)受体阻滞剂所抑制。因此，应激诱导的淋巴细胞募集，特别是NK细胞的募集，是由肾上腺素通过激活淋巴细胞上的β受体而介导的。
To evaluate stress-induced changes in blood leukocytes with emphasis on the natural killer (NK) cells, eight male volunteers were followed during three trials of head-up tilt with adrenergic beta(1)-(metoprolol) and beta(1+2)- (propranolol) blockade and with saline (control) infusions. The beta(1)- and beta(1+2)-receptor blockade did not affect the appearance of presyncopal symptoms, but the head-up tilt induced a transient lymphocytosis that was abolished by beta(1+2)-receptor blockade but not by beta 1-receptor blockade. Head-up tilt also resulted in delayed neutrophilia, which was insensitive to beta-receptor blockade. Lymphocyte subset analysis revealed that the head-up tilt resulted in a twofold increase in the percentage and absolute number of CD3(-)/CD16(+) and CD3(-)/CD56(+) NK cells in peripheral blood and that this increase was partially blocked by metoprolol and abolished by propranolol. The NK cell activity on a per NK cell basis did not change during head-up tilt, indicating that the cytotoxic capability of NK cells recruited to circulation is unchanged. The data suggest that the head-up tilt-induced lymphocytosis was due mainly to CD16(+) and CD56(+) NK cells and that their recruitment to the blood was inhibited by beta 1- and especially beta(1+2)-receptor blockade. Thus stress-induced recruitment of lymphocytes, and of NK cells in particular, is mediated by epinephrine through activation of beta-receptors on the lymphocytes.