Pulmonary vasoreactivity to serotonin during hypoxia is modulated by ATP-sensitive potassium channels

The role of ATP-sensitive K+-channel modulation in the canine pulmonary vascular response to serotonin during hypoxia was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured by using vascular occlusion techniques. Under normoxia, serotonin (10(-5) M) significantly increased precapillary and postcapillary resistances and pulmonary capillary pressure and decreased total vascular compliance by decreasing both microvascular and large-vessel compliances. During hypoxia, the effect of serotonin was potentiated on both precapillary and postcapillary resistance and capillary pressure, as well as on microvascular compliance and large-vessel compliance. Under normoxia, the ATP-sensitive K+-channel opener cromakalim (10(-5) M) inhibited the serotonergic response on postcapillary resistance and microvascular compliance, whereas during hypoxia cromakalim inhibited the potentiated effect of serotonin on both precapillary and postcapillary resistance, capillary pressure, and both microvascular and large-vessel compliances. These results indicate that canine pulmonary vasoreactivity to serotonin is heightened under hypoxic conditions and that ATP-sensitive K+ channels modulate the presser response to serotonin, an effect that is more pronounced during hypoxia.