Naloxone decreases the inhibitory effect of somatostatin on GH release induced by cigarette smoking in man

• Published in: Journal of Neural Transmission Vol. 118; no. 8; pp. 1173 - 1175
• Main Authors: Coiro, Vittorio, Volpi, Riccardo, Stella, Adriano, Cataldo, Simona, Giumelli, Claudio, Maccanelli, Francesco, Araldi, Anna, Chiodera, Paolo
• Format: Journal Article
• Language: English
• Published: Vienna Springer Vienna 01.08.2011; Springer Nature B.V
• Subjects: Adult; Basic Neurosciences; Genetics and Immunology - Rapid Communication; Human Growth Hormone - antagonists & inhibitors; Human Growth Hormone - blood; Human Growth Hormone - secretion; Humans; Male; Medicine; Medicine & Public Health; Naloxone - pharmacology; Neurology; Neurosciences; Psychiatry; Signal Transduction - drug effects; Signal Transduction - physiology; Smoking - blood; Somatostatin - antagonists & inhibitors; Somatostatin - pharmacology; Young Adult; GH; Naloxone; Somatostatin; Cigarette smoking
• ISSN: 0300-9564; 1435-1463
• DOI: 10.1007/s00702-011-0610-0

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.