The right atrium has been shown to mediate release of ACTH in response to small hemorrhage. Therefore, the authors sought to identify hypothalamic neurons (cat, α choloralose 35-45 mg/kg) whose firing rates were modulated by stretch of the right atrial vena caval junction. Stretch was produced by intermittent inflation of a balloon implanted between the pericardium and the right atrium. In some cases, carotid arteries were occluded bilaterally. Previous results indicate that electrical stimulation of the medial dorsal hypothalamus (MDH) causes prompt changes in ACTH, but stimulation in the lateral hypothalamus does not cause changes. Of 64 cells recorded in the MDH, 41 responded to atrial stretch. However, only 2 of 18 cells outside this region responded. Six cells were studied with and without carotid occlusion. The results suggest that integration of afferent signals from cardiovascular receptors occurs in the MDH and that the MDH may participate in neural medication of ACTH in response to hemodynamic changes.