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Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912
Received 14 November 1996; accepted in final form 4 April 1997.
Barman, Scott A. Pulmonary vasoreactivity to serotonin
during 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 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 pressor
response to serotonin, an effect that is more pronounced during
hypoxia.
adenosine 5
-triphosphate; pulmonary vascular resistance; pulmonary vascular compliance; pulmonary capillary pressure; cromakalim
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