Sympathectomy inhibits the vasoactive effects of nicotine in conscious rats

Objective: The mechanisms underlying the presser response to nicotine are i ncompletely understood. Although sympatho-adrenergic activation plays a maj or role, the relative contribution of adrenal vs, neurally released catecho lamines and the possible role of non-adrenergic factors (e.g. vasopressin r elease) is not established. Methods: We examined the cardiovascular respons es to graded i.v. injections of nicotine (1 to 100 mu g kg(-1)) in consciou s Wistar-Kyoto rats under control conditions and (i) after chemical sympath ectomy by 6-hydroxydopamine, which destroys sympathetic endings but spares the adrenal medulla; (ii) after an alpha-adrenergic blockade by phenoxybenz amine; (iii) after a V-1 vasopressin receptor blockade by a specific antago nist. Results: In control rats, nicotine caused a dose-dependent tachycardi ac and presser response. Both responses were abolished by sympathectomy, wh ereas the alpha-blockade left the tachycardiac response unaffected but inhi bited the presser response; the V-1 vasopressin receptor blockade had no ef fect on either the tachycardiac or presser response. Conclusions: We conclu de that in the conscious rat: (1) the presser response to nicotine mainly d epends on peripheral alpha-adrenergically-mediated vasoconstriction; (2) th e vasomotor effect is caused by neural rather than adrenomedullary catechol amine release; (3) the nicotine-induced increase in heart rate (and presuma bly cardiac output) is per se unable to raise blood pressure, and (4) the n icotine-induced release of vasopressin plays no significant role in the pre sser response. (C) 1999 Elsevier Science B.V. All rights reserved.