Differential Effect of Calcium-Activated Potassium and Chloride Channels on Rat Basilar Artery Vasomotion

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences Vol. 34; no. 4; pp. 482 - 490
• Main Author: 李丽 王蕊 马克涛 李新芝 张传林 刘卫东 赵磊 司军强
• Format: Journal Article
• Language: English
• Published: Heidelberg Huazhong University of Science and Technology 01.08.2014; Department of Physiology, Medical College of Shihezi University, Shihezi 832002, China; The Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Medical College of Shihezi University, Shihezi 832002, China%Department of Physiology, Medical College of Shihezi University, Shihezi 832002, China%Department of Physiology, Medical College of Shihezi University, Shihezi 832002, China; Department of Neurobiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China; The Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Medical College of Shihezi University, Shihezi 832002, China
• Subjects: Animals; Basilar Artery - cytology; Basilar Artery - metabolism; Basilar Artery - physiology; Chloride Channels - metabolism; Female; Male; Medicine; Medicine & Public Health; Membrane Potentials - physiology; Muscle, Smooth, Vascular - cytology; Muscle, Smooth, Vascular - metabolism; Myocytes, Smooth Muscle - cytology; Myocytes, Smooth Muscle - metabolism; Potassium Channels, Calcium-Activated - metabolism; Rats; Rats, Wistar; Vasoconstriction - physiology; Vasodilation - physiology; 动脉血管; 基底动脉; 大鼠; 工作压力; 氯通道; 激活; 血管平滑肌细胞; 钙通道; basilar artery; vasomotion; gap junction; vascular smooth muscle cell; calcium-activated ion channels; pressure myograph
• ISSN: 1672-0733; 1993-1352
• DOI: 10.1007/s11596-014-1303-3

Spontaneous, rhythmical contractions, or vasomotion, can be recorded from cerebral vessels under both normal physiological and pathophysiological conditions. We investigated the cellular mechanisms underlying vasomotion in the cerebral basilar artery （BA） of Wistar rats. Pressure myograph video microscopy was used to study the changes in cerebral artery vessel diameter. The main results of this study were as follows： （1） The diameters of BA and middle cerebral artery （MCA） were 314.5±15.7 μm （n=15） and 233.3±10.1 μm （n=12） at 10 mmHg working pressure （P〈0.05）, respectively. Pressure-induced vasomotion occurred in BA （22/28, 78.6%）, but not in MCA （4/31, 12.9%） from 0 to 70 mmHg working pressure. As is typical for vasomotion, the contractile phase of the response was more rapid than the relaxation phase; （2） The frequency of vasomotion response and the diameter were gradually increased in BA from 0 to 70 mmHg working pressure. The amplitude of the rhythmic con- tractions was relatively constant once stable conditions were achieved. The frequency of contractions was variable and the highest value was 16.7±4.7 （n=13） per 10 min at 60 mmHg working pressure; （3） The pressure-induced vasomotion of the isolated BA was attenuated by nifedipine, NFA, 181]-GA, TEA or in Ca2＋-free medium. Nifedipine, NFA, 18~-GA or Ca2＋-free medium not only dampened vasomotion, but also kept BA in relaxation state. In contrasts, TEA kept BA in contraction state. These results sug- gest that the pressure-induced vasomotion of the isolated BA results from an interaction between Ca2＋-activated C1- channels （CaCCs） currents and Kca currents. We hypothesize that vasomotion of BA depends on the depolarizing of the vascular smooth muscle cells （VSMCs） to activate CaCCs. Depolarization in turn activates voltage-dependent Ca2＋ channels, synchronizing contractions of adjacent cells through influx of extracellular calcium and the flow of calcium through gap junctions. Subsequent calcium-induced calcium release from ryanodine-sensitive stores activates Kca channels and hyperpo- larizes VSMCs, which provides a negative feedback loop for regenerating the contractile cycle.