title: Differential effect of calcium-activated potassium and chloride channels on rat basilar artery vasomotion.
abstract: 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 contractions 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, 18β-GA, TEA or in Ca(2+)-free medium. Nifedipine, NFA, 18β-GA or Ca(2+)-free medium not only dampened vasomotion, but also kept BA in relaxation state. In contrasts, TEA kept BA in contraction state. These results suggest that the pressure-induced vasomotion of the isolated BA results from an interaction between Ca(2+)-activated Cl(-) channels (CaCCs) currents and K(Ca) 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 Ca(2+) 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 K(Ca) channels and hyperpolarizes VSMCs, which provides a negative feedback loop for regenerating the contractile cycle.
authors.affiliation: 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.
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, 832002, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Wang
authors.affiliation: 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.
authors.forename: Ke-Tao
authors.initials: KT
authors.lastname: Ma
authors.affiliation: 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 Neurobiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
authors.forename: Xin-Zhi
authors.initials: XZ
authors.lastname: Li
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, 832002, China.
authors.forename: Chuan-Lin
authors.initials: CL
authors.lastname: Zhang
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, 832002, China.
authors.forename: Wei-Dong
authors.initials: WD
authors.lastname: Liu
authors.affiliation: 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.
authors.forename: Lei
authors.initials: L
authors.lastname: Zhao
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, 832002, China. sijunqiang11@hotmail.com.|The Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Medical College of Shihezi University, Shihezi, 832002, China. sijunqiang11@hotmail.com.|Department of Neurobiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. sijunqiang11@hotmail.com.|Department of Physiology, Wuhan University School of Basic Medical Sciences, Wuhan, 430070, China. sijunqiang11@hotmail.com.
authors.forename: Jun-Qiang
authors.initials: JQ
authors.lastname: Si
mesh_terms: D000818:Animals; D001488:Basilar Artery / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D018118:Chloride Channels / Q000378:metabolism*; D005260:Female; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism*; D032389:Myocytes, Smooth Muscle / Q000166:cytology / Q000378:metabolism*; D024681:Potassium Channels, Calcium-Activated / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D014661:Vasoconstriction / Q000502:physiology*; D014664:Vasodilation / Q000502:physiology*
chemical_list: D018118:Chloride Channels; D024681:Potassium Channels, Calcium-Activated