GENETIC ABLATION OF CALCIUM-INDEPENDENT PHOSPHOLIPASE A(2)BETA

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 磷脂酶的激活导致花生四烯酸和溶血磷脂的释放，这两种物质在调节血管舒张性张力方面发挥着重要作用。为了确定钙非依赖性磷脂酶A(2)β(iPLA(2)beta)在血管运动功能中的作用，我们测量了野生型(WT；ipla(2)beta(+/+))和缺乏β-异构体(ipla(2)beta(-/-))小鼠肠系膜小动脉对苯肾上腺素(PE)和ACh的血管反应。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Activation of phospholipases leads to the release of arachidonic acid and lysophospholipids that play prominent roles in regulating vasomotor tone. To identify the role of calcium-independent phospholipase A(2)beta (iPLA(2)beta) in vasomotor function, we measured vascular responses to phenylephrine (PE) and ACh in mesenteric arterioles from wild-type (WT; iPLA(2)beta(+/+)) mice and those lacking the beta-isoform (iPLA(2)beta(-/-)) both ex vivo and in vivo.