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  • Title: Sympathectomy inhibits the vasoactive effects of nicotine in conscious rats.
    Author: Marano G, Ramirez A, Mori I, Ferrari AU.
    Journal: Cardiovasc Res; 1999 Apr; 42(1):201-5. PubMed ID: 10435011.
    Abstract:
    OBJECTIVE: The mechanisms underlying the pressor response to nicotine are incompletely understood. Although sympatho-adrenergic activation plays a major role, the relative contribution of adrenal vs. neurally released catecholamines and the possible role of non-adrenergic factors (e.g. vasopressin release) is not established. METHODS: We examined the cardiovascular responses to graded i.v. injections of nicotine (1 to 100 micrograms kg-1) in conscious Wistar-Kyoto rats under control conditions and (i) after chemical sympathectomy by 6-hydroxydopamine, which destroys sympathetic endings but spares the adrenal medulla; (ii) after an alpha-adrenergic blockade by phenoxybenzamine; (iii) after a V1 vasopressin receptor blockade by a specific antagonist. RESULTS: In control rats, nicotine caused a dose-dependent tachycardiac and pressor response. Both responses were abolished by sympathectomy, whereas the alpha-blockade left the tachycardiac response unaffected but inhibited the pressor response: the V1 vasopressin receptor blockade had no effect on either the tachycardiac or pressor response. CONCLUSIONS: We conclude that in the conscious rat; (1) the pressor response to nicotine mainly depends on peripheral alpha-adrenergically-mediated vasoconstriction; (2) the vasomotor effect is caused by neural rather than adrenomedullary catecholamine release; (3) the nicotine-induced increase in heart rate (and presumably cardiac output) is per se unable to raise blood pressure, and (4) the nicotine-induced release of vasopressin plays no significant role in the pressor response.
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