Electrical properties of resting and acetylcholine‐stimulated endothelium in intact rat aorta.
Electrical properties of resting and acetylcholine‐stimulated endothelium in intact rat aorta.
复制标题
完整大鼠主动脉静息和乙酰胆碱刺激内皮的电特性。
DOI：
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
S. Sage
中科院分区：
文献类型：
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作者：
S. Marchenko;S. Sage
1.采用膜片钳全细胞模式研究了大鼠主动脉内皮细胞的被动电特性及乙酰胆碱对内皮细胞膜电位的影响。2.未受刺激的内皮具有-58 +/-8 mV的膜电位（S.E.M.，n = 193;范围-47至-76 mV）。输入电阻为43 +/-13 M Ω（S.E.M.，n = 8;范围26 - 64 M Ω）。KCl和BaCl 2可使内皮去极化，但四乙基铵（2 mM）、4-氨基吡啶（5 mM）或4，4 '-二异硫氰酸基芪-2，2'-二磺酸（DIDS; 100 μ M）不能。3.乙酰胆碱（0.2 - 4 μ M）在大多数制备物中引起双相反应，瞬时超极化至接近K+逆转电位的值，随后去极化超过静息电位。在46%的记录中，去极化之后是膜电位的振荡。在给定主动脉的所有记录中，超极化的持续时间和去极化的幅度相似，但不同制剂之间差异很大。4.低于K+逆转电位的内皮超极化逆转了乙酰胆碱诱发反应的第一相的方向，这不受四乙基铵、4-氨基吡啶或DIDS的影响。5.细胞外Ca 2+的去除引起内皮的去极化从-61 +/-3 mV到-34 +/-3 mV（S.E.M.，n = 9）2 - 15 min。恢复外部Ca 2+引起短暂超极化。6.在去除Ca 2+后不久，在名义上无Ca（2+）的培养基中应用ACh仅引起短暂的超极化。在无Ca（2+）培养基中建立稳定的膜电位后，乙酰胆碱没有影响。7. NiCl 2（2 mM）引起内皮细胞的小去极化（6 +/-2 mV; S.E.M.，n = 7）。随后去除Ni 2+诱发了短暂的超极化。8.在Ni 2+存在下，乙酰胆碱诱发短暂的超极化。Ni 2+的应用和细胞外Ca 2+的去除立即阻断乙酰胆碱引起的膜电位振荡。9.电压操作性钙通道阻滞剂硝苯地平（1 - 10 μ M）和维拉帕米（20 μ M）对双相乙酰胆碱诱发反应无影响。10.在乙酰胆碱引起膜电位大幅度（20 - 45 mV）振荡的制剂中，单独通过电流注射或应用KCl对内皮细胞进行去极化不会引起振荡。11.蛋白激酶C的激活剂佛波醇12，13-二丁酸酯（200 nM）去极化并大大增加了内皮的输入阻力，可能是由于对间隙连接的影响。（400字处截断摘要）
1. The passive electrical properties and the effects of acetylcholine on the membrane potential of the endothelium of intact rat aorta were investigated using the whole cell mode of the patch clamp technique. 2. Unstimulated endothelium had a membrane potential of ‐58 +/‐ 8 mV (S.E.M., n = 193; range ‐47 to ‐76 mV). The input resistance was 43 +/‐ 13 M omega (S.E.M., n = 8; range 26‐64 M omega). KCl and BaCl2, but not tetraethylammonium (2 mM), 4‐aminopyridine (5 mM) or 4,4'‐diisothiocyanatostilbene‐2,2'‐disulphonic acid (DIDS; 100 microM) depolarized the endothelium. 3. Acetylcholine (0.2‐4 microM) evoked in most preparations a biphasic response with a transient hyperpolarization to a value close to the K+ reversal potential, followed by depolarization beyond the resting potential. In 46% of recordings, the depolarization was followed by oscillations in membrane potential. The duration of the hyperpolarization and magnitude of the depolarization was similar in all recordings from a given aorta, but varied greatly between different preparations. 4. Hyperpolarization of the endothelium below the K+ reversal potential reversed the direction of the first phase of the acetylcholine‐evoked response, which was unaffected by tetraethylammonium, 4‐aminopyridine, or DIDS. 5. The removal of extracellular Ca2+ evoked a depolarization of the endothelium from ‐61 +/‐ 3 to ‐34 +/‐ 3 mV (S.E.M., n = 9) over 2‐15 min. Restoration of external Ca2+ evoked a transient hyperpolarization. 6. ACh applied in nominally Ca(2+)‐free medium shortly after Ca2+ removal evoked only a transient hyperpolarization. After the establishment of a stable membrane potential in Ca(2+)‐free medium, acetylcholine was without effect. 7. NiCl2 (2 mM) evoked a small depolarization of the endothelium (6 +/‐ 2 mV; S.E.M., n = 7). The subsequent removal of Ni2+ evoked a transient hyperpolarization. 8. In the presence of Ni2+, acetylcholine evoked a short‐lived hyperpolarization. Both the application of Ni2+ and the removal of extracellular Ca2+ immediately blocked oscillations in membrane potential evoked by acetylcholine. 9. The blockers of voltage‐operated Ca2+ channels, nifedipine (1‐10 microM) and verapamil (20 microM) were without effect on the biphasic acetylcholine‐evoked responses. 10. In preparations in which acetylcholine evoked large (20‐45 mV) oscillations in membrane potential, depolarization of the endothelium alone, by current injection or application of KCl, did not evoke oscillations. 11. The activator of protein kinase C, phorbol 12, 13‐dibutyrate (200 nM) depolarized and greatly increased the input resistance of the endothelium, presumably due to an effect on gap junctions.(ABSTRACT TRUNCATED AT 400 WORDS)
切除的大鼠颈动脉中内皮细胞的保存。
影响因子：
20.1
作者：
Lewis,DA;Loomis,JL;Segal,SS
通讯作者：
Segal,SS
影响因子：
2.6
作者：
JOHNS, A;LATEGAN, TW;ADAMS, DJ
通讯作者：
ADAMS, DJ