SUMMARY Previous studies have implicated the area postrema (AP) as a site responsible for the centrally mediated neurogenic effects of angiotensin II. To clarify its role further we characterized in mongrel dogs: 1) the onset and offset transients of the pressor response due to electrical stimulation of the AP; 2) the peripheral efferent autonomic pathways; and 3) the immediate and long-term hemodynamic effects of AP ablation. Large pressor responses (+30 ± 4 mm Hg) due to increased peripheral resistance were obtained at low stimulus strength (20-80 MA) via electrodes stereotaxically lowered into the area postrema. Rises in arterial pressure were due to augmented sympathetic activity because they were prevented by sympathetic ganglionic blockade. and were unaffected by either vagotomy or beta-adrenergic blockade. In conscious, trained, instrumented dogs thermocoagulation of the AP caused transient hypertension (40 ± 1%) and tachycardia. Subsequently, mild hypotension due to decreases in cardiac output and peripheral resistance was a feature persisting for 4 additional weeks of measurements. The mild changes in resting hemodynamics were associated with a large fall in the normal lability of heart rate and cardiac output sustained for the entire period of observation. The hypotensive effects of AP ablation were accompanied by significantly reduced vasoconstrictor effects of I.V. injected angiotensin II at all doses tested (0.5-5 fig). Vascular responses to I.V. norepinephrine (5-40 ng) were augmented. Since electrical stimulation causes hypertension and ablation results in sustained hypotension, the data indicate that the AP participates in the regulation of blood pressure by the central nervous system.