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  • Title: Rapid and discrete changes in hypothalamic catecholamine nerve terminal systems induced by audiogenic stress, and their modulation by nicotine-relationship to neuroendocrine function.
    Author: Siegel RA, Andersson K, Fuxe K, Eneroth P, Lindbom LO, Agnati LF.
    Journal: Eur J Pharmacol; 1983 Jul 15; 91(1):49-56. PubMed ID: 6617738.
    Abstract:
    The effects of acute audiogenic stress, with or without simultaneous nicotine treatment (0.3 mg/kg i.v.), on catecholamine levels in discrete dopamine and noradrenaline nerve terminal systems of the hypothalamus, and on the secretion of adenohypophyseal hormones and of corticosterone, were studied using quantitative microfluorometric evaluations of catecholamine stores and radioimmunoassays for the determination of serum hormone levels. Audiogenic stress and nicotine induced very rapid and discrete decreases in noradrenaline levels in the subependymal layer (SEL), in the parvocellular part of nuc. paraventricularis hypothalamic (PA FP) and in the posterior periventricular hypothalamic systems, (PV II); the decreases were apparent 2 min following the onset of treatment. Increases of arterial blood pressure were observed after nicotine treatment but could not have been a major factor in producing the changes in catecholamine levels. These changes in NA levels may be related to the nicotine- and stress-induced increases of ACTH (SEL and PA FP) and prolactin secretion (PV II) found in the present experiments. Stress enhanced the rapid but variable increase in vasopressin secretion induced by nicotine, suggesting one possible mechanism by which stress combined with smoking can contribute to the development of increased arterial blood pressure and finally to sustained hypertension.
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