Endocrine Abstracts

Introduction and objectives: The inhalation of tobacco smoke leads to an acute increase in cortisol, ACTH and GH concentration, both in chronic smokers as in non-smokers. However, most studies have failed to demonstrate differences between both groups in basal levels of these hormones in plasma or urine. Additionally, cholinergic pathways have been shown to play an inhibitory role in ACTH secretion in non-smokers. UFC and circulating levels of cortisol, ACTH and GH were evaluated basally and after pyridostigmine in smokers and non-smokers.

Subjects and methods: We studied UFC (urinary free cortisol) on 24 h urine samples and the effects of administration of placebo and pyridostigmine on ACTH, cortisol and GH secretion in 10 young males: five smokers and five non-smokers. In each test, placebo or pyridostigmine (120 mg) were given orally in random order on different days at 0830. Blood samples were drawn at 0830, 0900 and then every 15 min until 1130. Area under the curve was calculated. Data are expressed as mean ± SEM.

Results: Basal levels of UFC, plasma ACTH, and serum GH were not different between smokers and non-smokers. In contrast, basal serum cortisol was higher in smokers at 1015 (15.42±1.38 vs 10.29±1.40 mcg/dl) and 1045 (12.96±1.14 vs 8.89±1.19 mcg/dl). PD raised GH secretion within each group, while it decreased cortisol at 1015 (15.42±1.38 vs 13.20±1.50 mcg/dl) in smokers and ACTH at 1115 (16.87±1.54 vs 12.49±1.65 pg/ml) in non-smokers.

Conclusions: Chronic smoking is associated with increased basal serum cortisol and normal UFC, while it is related to a decrease in serum cortisol after pyridostigmine. Besides, an inhibitory effect of cholinergic stimulation on ACTH is confirmed in non-smokers.