REGULATION OF ARTERIAL TONE BY ACTIVATION OF CALCIUM-DEPENDENT POTASSIUM CHANNELS
REGULATION OF ARTERIAL TONE BY ACTIVATION OF CALCIUM-DEPENDENT POTASSIUM CHANNELS
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DOI：
10.1126/science.1373909
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发表时间：
1992-04-24
期刊：
影响因子：
56.9
通讯作者：
NELSON, MT
中科院分区：
文献类型：
--
作者：
BRAYDEN, JE;NELSON, MT
血压和组织灌注部分由内在（肌源性）血管张力水平控制。然而，这种反应的许多分子决定因素是未知的。现在有证据表明，肌原性张力的程度部分是由动脉平滑肌中大电导钙激活钾通道的激活调节的。四乙基铵离子（TEA+）和白垩纪毒素（CTX）的浓度可阻断从脑动脉分离的平滑肌细胞中钙活化的钾通道，导致脑动脉去极化和收缩。当通过降低血管内压力或阻断钙通道来减少细胞内钙时，TEA+和CTX对动脉的影响都很小。通过膜去极化引起的血管内压力升高和细胞内钙的增加可能激活钙活化的钾通道。因此，这些通道可能作为负反馈途径来控制膜去极化和血管收缩的程度。
Blood pressure and tissue perfusion are controlled in part by the level of intrinsic (myogenic) vascular tone. However, many of the molecular determinants of this response are unknown. Evidence is now presented that the degree of myogenic tone is regulated in part by the activation of large-conductance calcium-activated potassium channels in arterial smooth muscle. Tetraethylammonium ion (TEA+) and charybdotoxin (CTX), at concentrations that block calcium-activated potassium channels in smooth muscle cells isolated from cerebral arteries, depolarized and constricted pressurized cerebral arteries with myogenic tone. Both TEA+ and CTX had little effect on arteries when intracellular calcium was reduced by lowering intravascular pressure or by blocking calcium channels. Elevation of intravascular pressure through membrane depolarization and an increase in intracellular calcium may activate calcium-activated potassium channels. Thus, these channels may serve as a negative feedback pathway to control the degree of membrane depolarization and vasoconstriction.