The effects of cumulative doses of seven arteriolar vasodilators were examined in cats anesthetized with pentobarbital. Cardiac output was measured by a thermodilution technique and hepatic venous compliance by plethysmography. All the drugs produced dose-related decreases in total peripheral resistance. Diazoxide, prazosin, and sodium nitroprusside produced no significant changes in hepatic venous compliance or cardiac output. Diazoxide and prazosin produced no change in right atrial pressure, while nitroprusside produced a small fall. It is concluded that these drugs do not alter hepatic venous tone, although nitroprusside may cause a small venodilator effect elsewhere. Epinephrine and dopamine produced marked decreases in hepatic venous compliance and increased cardiac output. This increased cardiac output can be explained on the basis of cardiac stimulation combined with no increase in afterload due to arteriolar vasodilatation and maintenance of preload by venoconstriction. Isoproterenol and hydralazine unexpectedly produced a similar pattern--marked decreases in hepatic venous compliance and increased cardiac output. With hydralazine, these effects preceded arterial hypotension. Possible mechanisms are discussed. These studies support our roterenol and hydralazine produce a beta-receptor-mediated cardiac stimulation and an indirect hepatic venoconstriction, which are not secondary to the hypotension. Possible mechanisms are discussed. These studies support our hypothesis that splanchnic venoconstriction is a necessary factor for the production of large sustained increases in cardiac output. A reduction in afterload per se doesnot increase cardiac output in normal anesthetized cats since a compensatory decrease in preload occurs. It is suggested that afterload influences cardiac output only in situations where the heart is on the flat portion of the Starling function curve.