The present study was undertaken to evaluate the influence of respiratory condition [free breathing (FB) vs. controlled ventilation (CV)] and of anesthetic [pentobarbital (PA) vs. chloralose (CA)] on nicotine-induced vasomotor responses in the renal cortex and splanchnic beds. Nicotine (36 micrograms . kg-1 . min-1 iv) was infused in four groups of dogs: group I, PA and CV; group II, PA and FB; group III, CA and CV; group IV, CA and FB. Regional vascular conductances (VC) were calculated from regional blood flows measured with 15-microns radioactive microspheres. In group I, VC fell in renal cortex (-22%) and pancreas (-52%), increased in liver (hepatic arterial bed +130%), and did not change significantly in duodenum and spleen. In group III, VC fell to a greater extent in renal cortex, pancreas, duodenum, and spleen than in group I; VC in hepatic arterial bed did not change. In FB dogs (groups II and IV), nicotine caused marked hyperventilation, but decreases in VC in renal cortex, pancreas, and duodenum were similar to those in CV dogs. Results indicate that during intravenous infusion of nicotine 1) hyperventilation does not attenuate or reverse vasoconstriction in renal cortex, pancreas, or duodenum under either PA or CA, although it does in spleen under CA; 2) vasodilator mechanisms predominate over vasoconstrictor mechanisms in the hepatic arterial bed; and 3) vasoconstrictor responses in renal cortex, pancreas, duodenum, spleen, and liver are more pronounced under CA than under PA.