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2. Nicotine and the Neuroendocrine System

Nicotine has a number of effects on the neuroendocrine system. In 1961 Hokfelt demonstrated that cigarette smoking could increase plasma cortisol and urinary 17-hydroxy-corticosteroids (Fuxe, Andersson, Eneroth, Harfstrand, & Agnati, 1989). Following nicotine treatment there is a rapid rise of plasma beta-endorphin concentrations suggesting the possibility that nicotine can produce an opioid-mediated euphoria and analgesia. Some studies have shown that nicotine can also release vasopressin through activation of nicotinic cholinergic receptors located on the nerve cells of the supraoptic nucleus (Fuxe, et al., 1989). Other studies have indicated that the vasopressin releasing action of nicotine is considerable in the ventral surface of the medulla, the most sensitive structure within the distribution space of the carotids.

Vasopressin also modulates the immune system by its potent mitogenic activity on thymocytes and other influences via lymphocytes (Fuxe, et al., 1989).

Chronic exposure to nicotine has also been found to reduce prolactin secretion (Fuxe et al., 1989). Heavy cigarette-smoking women have lower basal prolactin levels, which may reduce the duration of the lactation period. Nicotine initially increases circulating luteinizing hormone and is followed by a substantial lowering of serum luteinizing hormone. After several days of nicotine treatment, higher amounts of thyroid hormone is secreted. In adult animals nicotine has an inhibitory effect on thyroid stimulating hormone. There may exist nicotinic cholinergic receptors within the hypothalamus which have both excitatory and inhibitory effects on growth hormone secretion.

Nicotine also has an affect on weight gain. Findings by Nicklas, Tomoyasu, Muir and Goldberg (1999) suggested that nicotine has a direct effect on adipose tissue metabolism by elevating circulating plasma leptin concentration. Leptin is expressed and secreted by adipocytes and is thought to regulate body fat stores through hypothalamic control of energy intake and expenditure. Research showed that smokers have a higher leptin level for a given basal metabolic index than nonsmokers.

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