Functional analysis of PAR-1 and search for novel G protein-coupled receptors in cerebral vasospasm

兔蛛网膜下腔出血（SAH）模型脑动脉PAR-1表达上调，对凝血酶的收缩反应明显增强。鞘内注射PAR-1拮抗剂可防止SAH后PAR-1的上调和对凝血酶收缩反应的增强。SAH后，凝血酶激活PAR-1，从而上调PAR-1的表达，最终导致兔脑动脉对凝血酶的收缩反应增加。在各种G蛋白偶联受体和这些激动剂中观察到受体表达的上调和激动剂诱导的收缩的增强。

The expression of PAR-1 was up-regulated and the contractile response to thrombin was markedly enhanced in the cerebral artery of rabbit subarachnoid hemorrhage (SAH) model. The intrathecal administration of a PAR-1 antagonist prevented the up-regulation of PAR-1 and the enhancement of the contractile responses to thrombin after SAH. Following SAH, thrombin activates PAR-1, thereby up-regulating the expression of PAR-1, which culminates in the increased contractile response to thrombin in the rabbit cerebral artery. The up-regulation of the receptor expression and the enhancement of the agonist-induced contraction were observed in various G protein-coupled receptors and these agonists.