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Am J Physiol Heart Circ Physiol 278: H2105-H2114, 2000;
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Vol. 278, Issue 6, H2105-H2114, June 2000

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

N. I. Gokina and J. A. Bevan

Department of Pharmacology, College of Medicine, The University of Vermont, Burlington, Vermont 05405

The role of Ca2+ mobilization from intracellular stores and Ca2+-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 Ca2+-activated Cl- channels. Histamine-evoked transient contraction in Ca2+-free solution was abolished by ryanodine or by caffeine-induced depletion of Ca2+ stores. Ryanodine slowed the development of depolarization induced by histamine in Ca2+-containing solution but did not affect its magnitude. In arteries treated with 1 mM Co2+, 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 Ca2+ mobilization from ryanodine-sensitive stores is involved in histamine-induced initial, but not sustained, depolarization and contraction. Ca2+-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.

intracellular calcium stores; ryanodine; calcium-activated chloride channels; 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid; niflumic acid; nonselective cation channels


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