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

Barman, Scott A. Pulmonary vasoreactivity to serotoninduring hypoxia is modulated by ATP-sensitive potassium channels. J. Appl. Physiol. 83(2): 569-574, 1997.The role of ATP-sensitive K⁺-channel modulation in thecanine pulmonary vascular response to serotonin during hypoxia wasdetermined in the isolated blood-perfused dog lung. Pulmonary vascularresistances and compliances were measured by using vascular occlusiontechniques. Under normoxia, serotonin(10⁵ M) significantlyincreased precapillary and postcapillary resistances and pulmonarycapillary pressure and decreased total vascular compliance bydecreasing both microvascular and large-vessel compliances. Duringhypoxia, the effect of serotonin was potentiated on both precapillaryand postcapillary resistance and capillary pressure, as well as onmicrovascular compliance and large-vessel compliance. Under normoxia,the ATP-sensitive K⁺-channelopener cromakalim (10⁵ M)inhibited the serotonergic response on postcapillary resistance andmicrovascular compliance, whereas during hypoxia cromakalim inhibitedthe potentiated effect of serotonin on both precapillary andpostcapillary 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-sensitiveK⁺ channels modulate the pressorresponse to serotonin, an effect that is more pronounced duringhypoxia.