Swelling-activated K fluxes in vascular endothelial cells: volume regulation via K-Cl cotransport and K channels.
Swelling-activated K fluxes in vascular endothelial cells: volume regulation via K-Cl cotransport and K channels.
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血管内皮细胞中肿胀激活的 K 通量：通过 K-Cl 共转运和 K 通道进行体积调节。
DOI：
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发表时间：
1993
影响因子：
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通讯作者：
W. O'Neill
中科院分区：
文献类型：
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作者：
P. Perry;W. O'Neill
研究了牛主动脉内皮细胞中负责调节体积减少（RVD）的钾外排途径。低渗肿胀导致布美他尼不敏感的86Rb流出量迅速和可逆地增加三倍。当NO3取代Cl时，肿胀激活的86Rb外排被抑制43%，这种Cl依赖性外排被1 mM速尿抑制。Cl替代和速尿均不能抑制等渗介质中Ca离子载体（A23187）刺激的外排。4,4'-二异硫氰二苯乙烯-2,2'-二磺酸盐也能抑制肿胀激活的86Rb外排，而二硝基二苯乙烯二磺酸盐则不能。细胞肿胀诱导了容量调节性K损失，这种损失在低渗培养基中是不完全的，但在加入布美他尼或细胞等渗肿胀时是完全和更快的。布美他尼存在时K的损失被速尿部分阻断。我们得出结论，两种独立的肿胀激活的钾通量介导主动脉内皮细胞的RVD：一种是与钾-氯共转运一致的cl依赖性、速尿敏感但布美他尼不敏感的通量，另一种是可能由K通道介导的cl非依赖性外排。
K efflux pathways responsible for regulatory volume decrease (RVD) were examined in bovine aortic endothelial cells. Hypotonic swelling produced a rapid and reversible threefold increase in bumetanide-insensitive 86Rb efflux. Swelling-activated 86Rb efflux was inhibited 43% when Cl was replaced with NO3, and this Cl-dependent efflux was inhibited by 1 mM furosemide. Neither Cl replacement nor furosemide inhibited the efflux stimulated by a Ca ionophore (A23187) in isotonic medium. Swelling-activated 86Rb efflux was also inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonate but not by dinitrostilbenedisulfonate. Cell swelling induced a volume-regulatory K loss that was incomplete in hypotonic medium but complete and more rapid when bumetanide was added or when cells were swollen isosmotically. K loss in the presence of bumetanide was partially blocked by furosemide. We conclude that two separate swelling-activated K fluxes mediate RVD in aortic endothelial cells: a Cl-dependent, furosemide-sensitive, but bumetanide-insensitive flux that is consistent with K-Cl cotransport, and a Cl-independent efflux that presumably is mediated by K channels.