In the conscious, undisturbed toad, Bufo marinus, pulmonary arterial blood flow increased during periods of lung ventilation and decreased in intervening periods of pulmonary apnea. In unidirectionally ventilated, anesthetized toads, lung inflation produced by increasing the outflow resistance to pulmonary gas flow to 3 cmH2O caused a significant increase in pulmonary arterial blood flow and a significant decrease in cutaneous arterial blood flow. Changes in flow were associated with reciprocal changes in calculated vascular resistance. Mean pulmocutaneous pressure and cardiac frequency did not change significantly. Thus lung inflation (in the absence of changes in the composition of intrapulmonary gases) increased the proportion of total pulmocutaneous flow routed to the lungs and decreased the proportion directed to the skin. Unidirectional ventilation with air + 5% CO2 at constant lung volume produced a significant decrease in pulmonary arterial blood flow, an increase in calculated pulmonary arterial flow resistance, and a small increase in the flow to the cutaneous artery. Concomitant mild hypoxia potentiated the effects of pulmonary hypercapnia, although hypoxia alone was less effective than hypercapnia alone in decreasing pulmonary flow. Pulmonary arterial blood flow was decreased by infusion of acetylcholine into the pulmocutaneous artery, but epinephrine had no effect on either the pulmonary or cutaneous artery at doses below those that produced systemic effects. Atropine blocked all changes in pulmonary arterial blood flow. This and other evidence suggest that calculated arterial resistance changes are due to reflex changes in the tone of vascular smooth muscle. Intrapulmonary CO2-sensitive mechanoreceptors possess appropriate response characteristics to mediate the afferent limb of the reflex.