SUMMARY Blood pressure (BP) and heart rate became derated when prostaglandin E, (PGE2) was infused into the cerebral rentrides of awake and anesthetized rats. Frequency of sympathetic neural firing was also increased. While the magnitude of the pressor responses was larger In spontaneously hypertensive rats (SHRs) than in normotensive ones (NTRs), the accompanying increases in sympathetic nerve firing were not significantly different. Pressor effects were appreciable within 2 minutes after the start of the PGE2Infusion but did not become maximal until 15 minutes later. By contrast, acceleration in sympathetic nerve firing was maximal within 2 minutes and then dwindled or remained stationary thereafter. Removal of sympathetic vasomotor tone by cervical section of the spinal cord abolished early phases without affecting subsequent peaks of the pressor response. The overall height of the pressor responses In hypophysectomlzed NTRs was half that in sham-operated controls. These results suggest that PGE2acts centrally to elevate BP by increasing not only the sympathetic discharge but perhaps also the secretion of bypophysial hormones, such as vasopressln. In light of previous studies showing that SHRs secrete more vasopressln, It was considered possible that their enhanced pressor responsiveness to PGE2could result from a greater release of endogenous vasopressln.