To generate quantitative data on the contribution of the area postrema (AP) to the pressor activity of angiotensin II (ANG II), the peptide (7 ng X kg-1 X min-1) was infused intravenously in 10 conscious dogs for 6 h before, and several weeks after, AP lesion. Mean arterial pressure (MAP) and heart rate (HR) were recorded continuously, and plasma renin activity (PRA), ANG II immunoreactivity (ANG II-IR), aldosterone (ALDO), arginine vasopressin (AVP), norepinephrine (NE), epinephrine (EPI), and serum Na+ and K+ were measured at 3 and 6 h. Three hours into the infusion, MAP averaged 123 +/- 2 compared with 96 +/- 2 mmHg for controls (P less than 0.01). The increases in pressure were associated with unchanged HR, but increased lability of MAP and HR. PRA fell, whereas plasma levels of ANG II-IR and ALDO rose. Plasma levels of AVP, NE, serum Na+ and K+ did not change, but plasma EPI was significantly elevated at 6 h. Removal of the AP produced mild hypotension and decreased lability. Within 8 to 21 days after AP ablation, a significant decrease in the plateau phase (3-6 h) of the ANG II pressor response was recorded in all dogs. The attenuation of the pressor effects was not sustained, since 4-7 wk after AP lesion, the increases in pressure were equivalent to those obtained during the control period. These data indicate that the AP participates in the production of the pressor response to intravenous infusion of ANG II in conscious dogs. However, in the absence of this structure, alternative mechanisms are brought into play to restore the loss of its function.(ABSTRACT TRUNCATED AT 250 WORDS)