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The role of Ca 2+  mobilization from intracellular stores and Ca 2+ -activated Cl −  channels in caffeine- and histamine-induced depolarization and contraction of the rabbit middle cerebral artery has been studied by recording membrane potential and isometric force. Caffeine induced a transient contraction and a transient followed by sustained depolarization. The transient depolarization was abolished by ryanodine, DIDS, and niflumic acid, suggesting involvement of Ca 2+ -activated Cl −  channels. Histamine-evoked transient contraction in Ca 2+ -free solution was abolished by ryanodine or by caffeine-induced depletion of Ca 2+  stores. Ryanodine slowed the development of depolarization induced by histamine in Ca 2+ -containing solution but did not affect its magnitude. In arteries treated with 1 mM Co 2+ , histamine elicited a transient depolarization and contraction, which was abolished by ryanodine. DIDS and niflumic acid reduced histamine-evoked depolarization and contraction. Histamine caused a sustained depolarization and contraction in low-Cl −  solution. These results suggest that Ca 2+  mobilization from ryanodine-sensitive stores is involved in histamine-induced initial, but not sustained, depolarization and contraction. Ca 2+ -activated Cl −  channels contribute mainly to histamine-induced initial depolarization and less importantly to sustained depolarization, which is most likely dependent on activation of nonselective cation channels.

Role of intracellular Ca2+ release in histamine-induced depolarization in rabbit middle cerebral artery