Figure 6.

Proposed mechanism of astrocytic ET-1 mediated cerebral vasospasm after SAH. GET-1 mice with over-expressed in ET-1 showed more severe neurological deficits and vasospasm after SAH. Increased astrocytic ET-1 during SAH induces cerebral vasospasm through the ETA receptor and mediated by PKC-α, which leads to dynfunction in the K+ channels. Administration of ETA receptor antagonist ABT-627 ameliorates the SAH-induced vasospasm. The impairment of NO system also exaggerates the vasospasm effect. Astrocytic ET-1 leads to more severe cerebral edema and BBB breakdown that further contributes to cerebral vasoconstriction. Vasopressin V1a receptor antagonist, SR 49059, significantly reduced the SAH-induced edema, suggesting that astrocytic ET-1 induces edema in SAH through vasopressin V1a receptor.

Yeung et al. BMC Neuroscience 2013 14:131   doi:10.1186/1471-2202-14-131
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