Insulin potentiates @entity1063 -induced vascular tone by activation of XXXX and @entity669 kinase.

@entity101 @entity6 @entity670 @entity95 @entity1359 @entity7131 @entity4515 @entity8446 @entity112 @entity669 @entity1063 @entity11616
Insulin might play a role in the @entity101 occurring in @entity6 . In addition, insulin has recently been shown to potentiate @entity1063 (NE) induced vascular tone. We used ring segments of the @entity95 facial artery mounted in a myograph to test the hypothesis that potentiation of NE-induced tone by insulin may be related to activation of @entity7131 ( @entity7131 ) and @entity669 kinase (TK). NE-induced contractions in the presence of @entity8446 were 200% (NE 0.1 and 0.3 microM), 252% (NE 1 microM), and 129% (NE 3 microM) of control. @entity8446 had no effect on NE (10 and 100 microM) induced contractions. The potentiation by insulin of NE-induced tone was not altered by endothelium removal and could be mimicked by @entity1359 ( @entity4515 , 0.1 microM). @entity112 -induced contractions were not altered by @entity8446 . Insulin potentiation of NE-induced tone was suppressed by pretreatment of the @entity95 facial artery with the @entity7131 inhibitor @entity11616 (0.1 microM) or the TK inhibitor @entity670 (10 microM). 45Ca2+ influx due to NE (3 microM) did not change in the presence of @entity8446 or @entity4515 (0.1 microM) despite a higher contractile response, so that wall force per unit of 45Ca2+ influx was increased by @entity8446 and @entity4515 (0.1 microM). Calphostin C (0.1 microM) and @entity670 (10 microM) both prevented the increase in wall force per unit of 45Ca2+ influx due to @entity8446 . Our study shows that insulin potentiates NE-induced tone through a TK- and @entity7131 -dependent mechanism.
