In control cerebral artery myocytes, local Ca2+ release events from the sarcoplasmic reticulum (Ca2+ sparks) activate large conductance Ca2+ activated (BK) K+ channels, causing membrane potential hyperpolarization, decreased voltage-dependent Ca2+ channel (VDCC) activity and decreased global cytosolic Ca2+. Following SAH, the frequency of Ca2+ sparks and therefore BK channel activity is decreased, promoting membrane potential depolarization, increased VDCC activity and increased global cytosolic Ca2+ levels.