© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Sympathectomy inhibits the vasoactive effects of nicotine in conscious rats
aLaboratorio di Farmacologia, Istituto Superiore di Sanitá, Viale Regina Elena 299, 00161 Roma, Italy
bCentro di Fisiologia Clinica e Ipertensione, Cattedra di Cardioangiologia Medica, Università di Milano; Ospedale Maggiore, and CNR, Milano, Italy
cDivisione di Cardioriabilitazione, Ospedale di Seregno, Az. Osp. Civ., Vimercate (MI), Italy
* Corresponding author. Tel.: +39-6-4990-2395; fax: 39-6-4938-7104. E-mail address: gmarano@net.iss.it (A.U. Ferrari)
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 µg 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 
-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 -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 -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.
KEYWORDS Nicotine; Blood pressure; Heart rate; Sympathectomy; Arginine–vasopressin; Adrenal catecholamines
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