SummaryTo define a mechanism for the pressor effects of thyrotropin-releasing hormone (TRH), we evaluated changes in mean blood pressure (MBP) when a synthetic form of TRH (0.1 mg/kg, i.v.) was injected into two types of comatose patients: vegetative and brain dead. The patients in the vegetative group (n = 7, age 58 ± 6) retained spontaneous respiration and brainstem function, whereas the brain-dead (BD) patients (n = 7, age 68 ± 4) lacked these functions. In the vegetative group, TRH caused significant increases in MBP (from 91 ± 8 mm Hg to 110 ± 10 mm Hg) at 2 min after the injection [p < 0.05, analysis of variance (ANOVA) with a Scheffe F-test]. In contrast, five of the seven BD patient showed no alterations in the measured parameter in response to the TRH injection. However, the remaining two BD patients, who had spinal reflexes, exhibited an elevation in MBP. In such BD patients, baroreceptor reflex function was virtually absent, suggesting that the blood pressure regulation mediating through the baroreceptor reflex system might be abolished. These results indicate that in comatose patients, the hemodynamic effects of TRH may differ depending on impairments in the central nervous system; the results support previous reports indicating a mediation of the central sympathetic nervous system in the development of pressor effects of TRH. Furthermore, because brain-dead patients with spinal reflexes showed hypertensive responses to TRH, there is a possibility that these responses may have resulted from an activation of TRH receptors in the spinal cord.