Neuroendocrine reactivity to nicotine in smokers

Abstract

The present study explored neuropeptide responses to nicotine from smoking. Habitual smokers smoked research cigarettes of known strength under controlled laboratory conditions while blood samples were withdrawn unobtrusively for subsequent biochemical analysis. To provide a metric that reflected total nicotine intake and total neurohormonal output, data were integrated over time. Subjects were relatively unresponsive in the low-nicotine (0.48 mg) condition. In the high-nicotine (2.87 mg) condition, there were significant positive correlations between integrated plasma nicotine and plasma arginine vasopressin (r = +0.985), its carrier protein neurophysin I (r = +0.944), and beta-endorphin-beta-lipotropin (r = +0.977), but not adrenocorticotropic hormone. Data from an experiment that used an extraction step to remove beta-lipotropin corroborated the functional relationship between plasma nicotine and beta-endorphin implied by the original findings. Taking into account recent research on the role of neuropeptides in the modulation of affective states and cognitive function as well as of other CNS activity, the present findings were interpreted as strengthening the hypothesis that nicotine-stimulated neuropeptide release provides positive reinforcement for smoking.

The functional mu opioid receptor (OPRM1) Asn40Asp variant predicts short-term response to nicotine replacement therapy in a clinical trial

“…6 Although the effects of nicotine on the opioid system in humans are more equivocal, 31,32 nicotine administration via cigarette smoking has been shown to produce dose-related increases in plasma beta-endorphin. 33 Based on previous data and the results of the present study, possible mechanisms for the effect of OPRM1 genetic variation on response to NRT can be considered. Nicotine increases central level of beta-endorphin, 6 and the Asp40 OPRM1 variant has a three-fold greater binding affinity of beta-endorphin by this receptor.…”

Circulating Insulin Concentrations, Smoking, and Alcohol Intake Are Important Independent Predictors of Leptin in Young Healthy Men

“…Both leptin (10) and smoking alter neuroendocrine function (64), cortisol (65), testosterone (66), and thyroid hormone levels (67,68). The precise mechanism by which smoking and alcohol intake act on the adipocyte to regulate leptin levels and the mechanism by which these effects on circulating leptin may affect human physiology will be the subject of future investigation.…”

Effects of Low- and High-Nicotine Cigarette Smoking on Mood States and the HPA Axis in Men

“…There has been relatively little attention to the temporal covariance between the endocrine, cardiovascular, and subjective effects of cigarette smoking. Early clinical endocrine studies of the hormonal effects of cigarette smoking were limited by the lack of sensitive and precise radioimmunoassays (RIAs) for ACTH (Pomerleau et al, 1983). Moreover, samples for ACTH and/or cortisol analysis usually were collected at relatively infrequent intervals, or as single daily samples (Seyler et al, 1984(Seyler et al, , 1986Baron et al, 1995;Pickworth and Fant, 1998;del Arbol et al, 2000), and plasma nicotine levels were seldom measured.…”