Abstract
Subarachnoid hemorrhage decreases the expression of ryanodine receptors and increases the expression of the immunophilin, FK506-binding protein (FKBP)12.6 in cerebrovascular smooth muscle cells, reducing the occurrence of Ca(2+) sparks, limiting negative feedback regulation of cerebrovascular tone and promoting vasospasm. However, given the large number of binding partners with which FKBP12.6 and related proteins interact, it appears likely that the altered expression of this immunophilin will have a broader impact on cerebrovascular smooth muscle function. In addition, the mechanisms responsible for the measured changes in expression of ryanodine receptors and FKBP12.6 yet remain unknown. These topics should prove to be fertile ground for future studies.
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