Cigarette smoking causes a generalized disturbance in adrenal cortical hormone levels (Baron et al., 1995). Whether this can be attributed to a smoking-induced decrease in the activity of either 21- or 11-beta-hydroxylase in the adrenal cortex, resulting in increased secretion of adrenal androgens, or to other mechanisms has not been clarified (Hautanen & Adlercreutz, 1993; Hautanen et al., 1993; Baron et al., 1995). However, peripherally mediated effects may also be important, as nicotine can act additively with ACTH to stimulate adrenal steroidogenesis (Fuxe et al., 1989).
Smokers have substantially higher serum levels of dehydroepiandrosterone (DHEA), its sulfate (DHEAS) and androstenedione (Hautanen et al., 1993; Field et al., 1994; Baron et al., 1995; al'Absi et al., 2003). There is also extensive evidence that cigarette smoking acutely increases circulating cortisol levels (Winternitz & Quillen, 1977; Wilkins et al., 1982; Seyler et al., 1984). Chronic smoking results in higher levels of plasma and salivary cortisol (Field et al., 1994; Baron et al., 1995); however, normal levels of urinary cortisol in smokers have also been reported (Yeh & Barbieri, 1989). A possible mechanism of this action of tobacco smoking is the stimulation of the release of catecholamines from the adrenal medulla, which may facilitate pituitary ACTH secretion (Reisine et al., 1984). Cessation of chronic smoking is associated with a subsequent significant decline in serum cortisol concentrations to nonsmokers' levels (Puddey et al., 1976).
Few studies have examined the effects of tobacco withdrawal on cortisol levels; an increase in cortisol levels has been found after 48 h abstinence compared to levels during ad libitum smoking (Hughes et al., 1988). Many of the nicotine withdrawal symptoms of smokers who try to quit seem to be the body's response to changes in cortisol levels (Hochberg et al., 2003).
In mice, cortisol seems to modulate some of the physiological and behavioural effects of nicotine (Caggiula et al., 1998). It also modulates the responsiveness of mice to nicotine, probably through a reduction in nicotine's access to, or actions at, its receptors, or by acting noncompetitively as allosteric inhibitors of the function of nicotine receptors (Fuxe et al., 1990; Pauly & Collins, 1993; Ke & Lukas, 1996). Whether cortisol also influences nicotine sensitivity in smokers is not known.
Smoking may alter physiological systems involved in the stress response. Smokers show attenuated cortisol and systolic blood pressure response to acute stressors when compared to nonsmokers. The extent to which absent cortisol response is due to an enhanced negative feedback caused by the higher basal cortisol concentrations or to attenuated sensitivity to stress-related physiological activation is not yet clear. Potential central mechanisms involved in the altered stress response include a reduction in the number or affinity of receptors mediating effects of nicotine in different central nervous system structures that integrate the neuroendocrine stress response (al'Absi et al., 2003). Chronic nicotine consumption may also lead to lower responses of other stress hormones (ACTH, prolactin, growth hormone) to a variety of stimuli (Kirschbaum et al., 1994).
Nicotine activates the sympathoadrenal system and increases the synthesis and release of noradrenaline and adrenaline into circulation, and also alters the bioavailability of dopamine (Pomerleau, 1992). Single and repeated injections of nicotine in rats increase the expression of tyrosine hydroxylase, a rate-limiting enzyme in the catecholamine biosynthetic pathway (Hiremagalur & Sabban, 1995).
Clin Endocrinol. 2004;61(6) © 2004 Blackwell Publishing
Cite this: Endocrine Effects of Tobacco Smoking - Medscape - Dec 01, 2004.