Lesions of the ventromedial hypothalamus (VMN) depress lordosis but increase ultrasonic vocalization in female hamsters. These changes are consistent with the behavioral incompatibility of lordosis and ultrasound production and suggest that the VMN coordinates short-term changes in these behaviors. In keeping with past results, unilateral lesions disrupted lordosis responses to contralateral flank stimulation. The change appeared within 15 min after the lesion and was much more rapid than the corresponding effect in rats. For hamsters, these findings support other evidence suggesting VMN mediation of somatosensory, not just hormonal, influences on lordosis. In a companion study, ultrasound rates became depressed within 15 min of bilateral lesion of the VMN, suggesting a role for the VMN in the short-term control of ultrasound production. Calling at later time intervals was facilitated by the lesions. The direction and time course of the lesion effects on lordosis and ultrasound production suggest that the VMN cannot easily account for the behavioral incompatibility of these 2 responses.