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

被引:13
作者
Gokina, NI [1 ]
Bevan, JA [1 ]
机构
[1] Univ Vermont, Coll Med, Dept Pharmacol, Burlington, VT 05405 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2000年 / 278卷 / 06期
关键词
cimetidine; nifedipine; low sodium; cobalt; voltage-dependent calcium channels; nonselective cation channels;
D O I
10.1152/ajpheart.2000.278.6.H2094
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 mu M) 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 mu M) 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.
引用
收藏
页码:H2094 / H2104
页数:11
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