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Am J Physiol Heart Circ Physiol 278: H2094-H2104, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 6, H2094-H2104, June 2000

Histamine-induced depolarization: ionic mechanisms and role in sustained contraction of rabbit cerebral arteries

N. I. Gokina and J. A. Bevan

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

The role of membrane depolarization in the histamine-induced contraction of the rabbit middle cerebral artery was examined by simultaneous measurements of membrane potential and isometric force. Histamine (1-100 µM) induced a concentration-dependent sustained contraction associated with sustained depolarization. Action potentials were observed during depolarization caused by histamine but not by high-K+ solution. K+-induced contraction was much smaller than sustained contraction associated with the same depolarization caused by histamine. Nifedipine attenuates histamine-induced sustained contraction by 80%, with no effect on depolarization. Inhibition of nonselective cation channels with Co2+ (100-200 µM) reversed the histamine-induced depolarization and relaxed the arteries but induced only a minor change in K+-induced contraction. In the presence of Co2+ and in low-Na+ solution, histamine-evoked depolarization and contraction were transient. We conclude that nonselective cation channels contribute to histamine-induced sustained depolarization, which stimulates Ca2+ influx through voltage-dependent Ca2+ channels participating in contraction. The histamine-induced depolarization, although an important and necessary mechanism, cannot fully account for sustained contraction, which may be due in part to augmentation of currents through voltage-dependent Ca2+ channels and Ca2+ sensitization of the contractile process.

cimetidine; nifedipine; low sodium; cobalt; voltage-dependent calcium channels; nonselective cation channels


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