The influence of chronic subcutaneous nicotine administration on aldosterone and corticosterone plasma concentrations and the plasma renin activity.
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Abstract
Since adrenocortical hormones and the renin-angiotensin system are capable of inducing defined pathophysiologic changes in the cardiovascular system, similar to those observed after nicotine, experiments were performed in rats to investigate the effect of chronic nicotine administration on the plasma concentrations of aldosterone (PAC) and corticosterone (PCC) and on the plasma renin activity (PRA). The administration of nicotine (0.5 or 1.0 mg/kg s.c. twice daily) over a period of 8 weeks did not significantly affect PCC. However, PAC showed a marked decrease, which did not appear to be the result of a nicotine-induced ACTH inhibition, since a similar decrease in PAC was observed after suppression of ACTH by dexamethasone. PAC in rats with hereditary diabetes insipidus was depressed by nicotine to the same extent as in control rats. This argues against nicotine-induced stimulation of ADH leading to extracellular volume expansion, the cause of the observed decrease in PAC. Further experiments were carried out in which nicotine was administered chronically over 4 weeks (implanted osmotic minipumps infusing 0.17 mg/kg) in rats in which the endogenous activity of the renin-angiotensin system was modified by either a low- or high-salt diet. Nicotine did not influence PRA in the low-sodium group, whereas in the high-sodium group PRA increased after nicotine. The data show that chronic nicotine administration in rats does not activate salt- and volume-retaining endocrine systems. Plasma aldosterone even decreased, except in animals kept on a high-sodium diet, in which an increase of PRA under nicotine was observed.(ABSTRACT TRUNCATED AT 250 WORDS)