Vasopressin impairs K and K channel function after brain injuryATP ca *

This study was designed to characterize the role of vasopressin in impaired pial artery dilation to activators of the ATP sensitive K (K ) and calcium sensitive K (K ) channel following fluid percussion brain injury (FPI) in newborn pigs equipped with a closed ATP ca cranial window. Topical vasopressin was coadministered with the K and K channel agonists cromakalim and NS1619 in a ATP ca 1 concentration approximating that observed in CSF following FPI. Vasopressin so administered attenuated pial artery dilation to these K channel activators under conditions of equivalent baseline diameter during non injury conditions (1361 and 2361 vs. 461 and 1062% 28 26 for cromakalim 10 , 10 M before and after vasopressin, respectively). Attenuated responses were fully restored when these agonists were coadministered with vasopressin and the vasopressin antagonist [l-(b-mercapto-b,b-cyclopentamethylene propionic acid) 2-(omethyl)-Tyr-AVP] (MEAVP). Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI and MEAVP preadministration partially prevented such impairment (1361 and 2361, sham control; 261 and 561, FPI; and 961 and 1562%, 28 26 FPI-MEAVP pretreated for responses to cromakalim 10 , 10 M, respectively). These data show that vasopressin blunts K and K ATP ca channel mediated cerebrovasodilation. These data suggest that vasopressin contributes to impaired K and K channel function after ATP ca brain injury.  2000 Elsevier Science B.V. All rights reserved. Theme: Disorders of the nervous system