Intracerebral or parenchymal arterioles play an important role in the regulation of both global and regional blood flow within the brain. Brain cortex lacks significant collateral sources of blood and thus is at risk if blood flow through parenchymal arterioles is restricted. Increasingly, evidence is accumulating that abnormal parenchymal arteriolar constriction contributes to the development of neurological deficits caused by subarachnoid hemorrhage (SAH). For example, parenchymal arterioles isolated from SAH model rats exhibit enhanced constriction in response to increased intravascular pressure. This increased pressure-dependent constriction or myogenic tone would result in a shift in the cerebral autoregulatory response and decreased cerebral perfusion. Here, we summarize our current knowledge regarding cellular mechanisms contributing to enhanced contractility of parenchymal arteriolar myocytes following SAH. Our studies demonstrated that SAH-induced membrane potential depolarization involving altered K(+) homeostasis leads to enhanced voltage-dependent Ca(2+) channel activity, increased smooth muscle cytosolic Ca(2+), and parenchymal arteriolar constriction. In summary, emerging evidence demonstrates that SAH can profoundly affect parenchymal arteriolar tone, promoting decreased cortical blood flow and compromised neuronal viability.