Potassium channels modulate cerebral autoregulation during acute hypertension.

Potassium channels modulate cerebral autoregulation during acute hypertension.
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DOI:
10.1152/ajpheart.2000.278.6.h2003
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发表时间:
2000-06
期刊:
American journal of physiology. Heart and circulatory physiology
影响因子:
--
通讯作者:
R. Paternò;D. Heistad;F. Faraci
R. Paternò;D. Heistad;F. Faraci
中科院分区:
其他
文献类型:
--
作者:
R. Paternò;D. Heistad;F. Faraci

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我们检验了这样一个假设,即在血压急性升高时,脑小动脉的收缩通过钾(K(+))通道的激活而减弱。我们测试了钙依赖性K(+)通道抑制剂[伊比利亚毒素(50 nM)和四乙基铵(TEA,1 mM)]对急性高血压期间小动脉直径变化的影响。在麻醉大鼠中使用颅窗测量脑小动脉的直径(基线直径= 46 +/- 2 μ m,平均值+/- SE)。通过静脉输注苯肾上腺素将动脉压从对照值96 +/- 1 mmHg升高至130、150、170和200 mmHg。动脉压从基线升高至130和150 mmHg时,脑小动脉直径降低5- 10%。动脉压的较大增加导致小动脉直径的较大增加(即,“自动调节的突破”)。当动脉压增加到170和200 mmHg时,伊比利亚毒素或TEA抑制小动脉直径的增加。在不存在和存在伊比利亚毒素的情况下,200 mmHg下小动脉直径的变化分别为20 +/- 3%和-1 +/- 4%。这些发现表明,钙依赖性K(+)通道在动脉压急性升高时减弱脑微血管收缩,并且高水平动脉压下小动脉直径的增加不仅仅是一种被动现象。
We tested the hypothesis that constriction of cerebral arterioles during acute increases in blood pressure is attenuated by activation of potassium (K(+)) channels. We tested the effects of inhibitors of calcium-dependent K(+) channels [iberiotoxin (50 nM) and tetraethylammonium (TEA, 1 mM)] on changes in arteriolar diameter during acute hypertension. Diameter of cerebral arterioles (baseline diameter = 46 +/- 2 microm, mean +/- SE) was measured using a cranial window in anesthetized rats. Arterial pressure was increased from a control value of 96 +/- 1 mmHg to 130, 150, 170, and 200 mmHg by intravenous infusion of phenylephrine. Increases in arterial pressure from baseline to 130 and 150 mmHg decreased the diameter of cerebral arterioles by 5-10%. Greater increases in arterial pressure produced large increases in arteriolar diameter (i.e., "breakthrough of autoregulation"). Iberiotoxin or TEA inhibited increases in arteriolar diameter when arterial pressure was increased to 170 and 200 mmHg. The change in arteriolar diameter at 200 mmHg was 20 +/- 3% and -1 +/- 4% in the absence and presence of iberiotoxin, respectively. These findings suggest that calcium-dependent K(+) channels attenuate cerebral microvascular constriction during acute increases in arterial pressure, and that increases in arteriolar diameter at high levels of arterial pressure are not simply a passive phenomenon.