In control rats, nicotine caused a dose-dependent tachycardiac and pressor response. Both responses were abolished by sympathectomy, whereas the α-blockade left the tachycardiac response unaffected but inhibited the pressor response; the V
1 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 a-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.
MARANO G.
(1) ; RAMIREZ A.
(2 3) ; MORI I.
(2 3) ; FERRARI A. U.
(2 3 4) ;
http://cat.inist.fr/?aModele=afficheN&cpsidt=1739277Cardiovascular research
ISSN 0008-6363
CODEN CVREAU
1999, vol. 42, no1, pp. 201-205 (18 ref.)