Department of Internal Medicine and Biomedical Sciences, University of Parma, Via A. Gramsci 14, 43126, Parma, Italy.
J Neural Transm (Vienna). 2011 Aug;118(8):1173-5. doi: 10.1007/s00702-011-0610-0. Epub 2011 Mar 1.
To establish whether somatostatin (SRIH) exerts its inhibitory effect on the nicotine-induced release of GH by interacting with an opioid pathway, normal volunteers were treated with naloxone during (2 no-filter) cigarettes smoking and with SRIH. Nicotine significantly increased serum GH levels about 3.5 fold. Naloxone alone did not change GH rise induced by cigarette smoking. The stimulatory effect of GH by nicotine was completely blocked by SRIH. In the presence of both SRIH and naloxone, GH levels rose 1.5 fold in response to nicotine. Since naloxone only partially reversed the inhibiting action of SRIH, only a partial involvement of opioid peptides in SRIH action might be supposed. Alternatively, SRIH and naloxone-sensitive opiates might produce this inhibiting effect on GH rise in response to cigarette smoking through independent pathways.
为了确定生长抑素(SRIH)是否通过与阿片途径相互作用对尼古丁诱导的 GH 释放产生抑制作用,正常志愿者在(2 个无滤嘴)香烟吸烟期间和 SRIH 治疗期间接受了纳洛酮治疗。尼古丁可使血清 GH 水平显著升高约 3.5 倍。纳洛酮单独不能改变香烟引起的 GH 升高。SRIH 完全阻断了 GH 由尼古丁引起的刺激作用。在 SRIH 和纳洛酮同时存在的情况下,GH 水平在尼古丁的作用下升高了 1.5 倍。由于纳洛酮仅部分逆转了 SRIH 的抑制作用,因此只能假定阿片肽仅部分参与 SRIH 作用。或者,SRIH 和纳洛酮敏感阿片类药物可能通过独立途径对吸烟引起的 GH 升高产生这种抑制作用。