The possible role of protein kinase C in chronic cerebral vasospasm after subarachnoid hemorrhage has been suggested for a decade. Experimental results in vitro or in animal models support that protein kinase C is involved in the prolonged contraction of cerebral arteries similar to cerebral vasospasm. Activation of protein kinase C may interact with other signaling pathways such as myosin-light chain kinase, nitric oxide, intracellular Ca2+, and more recently protein tyrosine kinase and its substrates such as mitogen-activated protein kinase. A protein kinase C network may be activated during cerebral vasospasm.