The aim of the study was to examine whether or not arginine vasopressin (AVP) might modulate cardiopulmonary functions by acting on the lateral area of the ventrolateral medulla (VLM) in the rat. The rat was anesthetized, bilaterally vagotomized, paralyzed, ventilated, and then placed on a stereotaxic instrument in a prone position. Activity of the phrenic nerve (PNA) was monitored at normocapnia and hypercapnia in hyperoxia. Microinjection of AVP into the lateral region of the VLM resulted in a brief apnea followed by a significant decrease in PNA amplitude and a concomitant significant increase in blood pressure. The inhibition of PNA with AVP treatment could be partly attenuated by hypercapnia but not by phentolamine. Both inhibition of PNA and pressor response with AVP microinjection into the lateral VLM were totally abolished after pretreatment with AVP V1A receptor antagonist. These results suggest that a vasopressinergic pathway projects to the lateral VLM and modulates cardiopulmonary functions via AVP V1A receptors on neurons within the lateral VLM.