Monday, June 30, 2008

Both responses were abolished by sympathectomy

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 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 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=1739277
Cardiovascular research ISSN 0008-6363 CODEN CVREAU

1999, vol. 42, no1, pp. 201-205 (18 ref.)