Mechanism of agonistic angiotensin II type I receptor autoantibody-amplified contractile response to XXXX in the isolated @entity35 thoracic aorta.

@entity10406 @entity1809 @entity9423 @entity1808 @entity15258 @entity4385 @entity1468 @entity460 @entity6164 @entity35
UNASSIGNED: Agonistic autoantibody to the angiotensin II type I receptor ( @entity1809 -AA) is highly associated with @entity1468 by increasing the sensitivity of @entity1808 during pregnancy in @entity35 , thus leading to @entity1468 . However, the mechanism underlying this phenomenon remains unclear. The purpose of this study was to observe @entity1809 -AA amplification of @entity1808 -induced vasoconstriction in @entity35 thoracic aortic rings. It was found that exposure to low concentrations of @entity1809 -AA (0.4 nM) caused a contraction of <5% of the maximal response to 60 mM @entity10406 . In addition, the @entity1808 -induced contractile response was amplified in the presence of a threshold contraction to @entity1809 -AA, as manifested by a leftward shift of the midpoint of the concentration-response curve with no change in the maximal response. These results showed that preincubation with low @entity1809 -AA could amplify the @entity1808 dose-response curve, and this amplification could be attenuated markedly by 0.1   M heptapeptide AFHYESQ. In @entity460 -free Krebs solution, 10   M of @entity15258 (an @entity9423 inhibitor) both blocked the @entity1809 -AA base contraction and completely abolished the amplification. Both 5   M of @entity4385 (a phospholipase C inhibitor) and 10   M of   V1-2 (an   @entity6164 inhibitor) could partially inhibit the @entity1808 -induced contractile response.   V1-2, but not @entity4385 , could completely inhibit the amplification response of @entity1809 -AA to @entity1808 . These results suggest that @entity1809 -AA is able to cause amplification response to @entity1808 probably via the @entity460 -independent protein kinase C pathway, which may provide a new therapy strategy for @entity1468 .
