缓激肽在冠状静脉内皮细胞中激活的多种离子机制

Jianben Song, D. Zawieja, H. Granger, A. H. Goodman, M. Davis
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引用次数: 2

摘要

在冠状动脉内皮中,缓激素(BK)通过刺激Ca2+内流调节血管舒张剂的产生。为了研究这一过程中涉及的离子电流,我们将BK (100 nM)应用于单个牛冠状静脉内皮细胞(CVEC),同时记录膜电位(Em)或全细胞电流与[Ca2+]i。未受刺激细胞的静息电位Er呈双峰分布(-70±9 mV, n = 26;-15±8mv, n = 30)。与Er无关,BK在Em变化的同时引起双相[Ca2+]i增加。当Er为负至-30 mV时,通常观察到去极化。当Er为正至-30 mV时,通常观察到瞬态超极化。在电压箝位下,[Ca2+]随着膜的超极化而增加,BK存在时,[Ca2+]i/ΔEm的比值Δ大于未刺激的细胞。许多,但不是全部,细胞表现出外向的钾离子电流,似乎是Ca2+依赖。当存在时,这种电流通常比其他电流占主导地位。
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Multiple Ionic Mechanisms Activated by Bradykinin in Coronary Venular Endothelial Cells
In coronary endothelium, bradykinin (BK) modulates production of vasodilators by stimulating Ca2+ influx. To examine the ionic currents involved in this process, we applied BK (100 nM) to single bovine coronary venular endothelial cells (CVEC) while recording membrane potential (Em) or whole-cell current simultaneously with [Ca2+]i. The resting potential (Er) of unstimulated cells was bimodally distributed (-70 ± 9 mV, n = 26; -15 ± 8 mV, n = 30). Irrespective of Er, BK evoked a biphasic [Ca2+]i increase simultaneously with a change in Em. When Er was negative to -30 mV, depolarizations were typically observed. When Er was positive to -30 mV, transient hyperpolarizations were typically observed. Under voltage clamp, [Ca2+], increased as the membrane hyperpolarized and the ratio Δ[Ca2+]i/ΔEm was greater in the presence of BK than in unstimulated cells. Many, but not all, cells exhibited an outward K+ current that appeared to be Ca2+ dependent. When present, this current typically predominated over other cu...
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