INCREASE IN CALCIUM-CHANNEL CURRENT BY BETA-ADRENOCEPTOR AGONISTS IN SINGLE SMOOTH-MUSCLE CELLS ISOLATED FROM PORCINE CORONARY-ARTERY
INCREASE IN CALCIUM-CHANNEL CURRENT BY BETA-ADRENOCEPTOR AGONISTS IN SINGLE SMOOTH-MUSCLE CELLS ISOLATED FROM PORCINE CORONARY-ARTERY
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DOI：
10.1111/j.1476-5381.1990.tb15852.x
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发表时间：
1990-07-01
影响因子：
7.3
通讯作者：
TOMITA, T
中科院分区：
文献类型：
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作者：
FUKUMITSU, T;HAYASHI, H;TOMITA, T
1. 使用全细胞钳法，通常使用含有 CsCl 的电极，在从猪冠状动脉新鲜分散的单细胞中研究儿茶酚胺（异丙肾上腺素和去甲肾上腺素）和毛喉素对膜电流的作用。 2.在正常克雷布斯溶液中，无论有或没有30mM四乙铵(TEA)和0.5mM 4-氨基吡啶，异丙肾上腺素(1-5μM)明显增加由膜去极化引起的内向电流，而不影响-80mV的保持电流。当用羟乙磺酸盐替代外部Cl-时，观察到相同的效果。用含 K+ 电极记录的外向电流不受异丙肾上腺素的显着影响。 3. 在存在 67 mM Ba2+ 和 30 mM TEA 的情况下，用含 CsCl 的电极记录的最大内向电流为 119.+-。电流大于 30 pA 的细胞中为 7 pA（平均值 .+-. s.e. 平均值，n = 90）。基于阈值电压、缓慢的衰减时间过程、产生失活所需的大去极化以及对 Ca2+ 通道拮抗剂尼卡地平的高敏感性，L 型 Ca2+ 通道被认为是这些电流的原因。 4.异丙肾上腺素和去甲肾上腺素增加了去极化脉冲引起的内向电流的幅度。最大内向电流增强了43.+-。 7% (n = 12) 为异丙肾上腺素，39 .+-。 10% 去甲肾上腺素 (n = 6)，浓度为 1 μM。这些作用被普萘洛尔强烈抑制，但酚妥拉明则不然。 Forskolin (10 μM) 也将电流增强到类似的程度。 5表明，刺激β-肾上腺素受体会增加猪冠状动脉中通过L型Ca2+通道的内向电流的幅度，并且细胞内环磷酸腺苷可能参与该作用。
1. The action of catecholamines (isoprenaline and noradrenaline) and forskolin on membrane currents was studied in single cells freshly dispersed from the pig coronary artery by use of the whole-cell clamp method, usually with electrodes containing CsCl. 2. In normal Krebs solution, with and without 30 mM tetraethylammonium (TEA) and 0.5 mM 4-aminopyridine, isoprenaline (1-5 .mu.M) clearly increased the inward currents elicited by membrane depolarization, without affecting the holding current at -80 mV. The same effect was observed when the external Cl- was replaced with isethionate. The outward current recorded with K+-containing electrodes was not significantly affected by isoprenaline. 3. In the presence of 67 mM Ba2+ and 30 mM TEA, the maximum inward current recorded with CsCl containing electrodes was 119 .+-. 7 pA (the mean .+-. s.e. mean, n = 90) in cells where the current was larger than 30 pA. The L-type Ca2+ channel was considered to be responsible for these currents, based on the threshold voltage, the slow time course of decay, the large depolarization necessary to produce inactivation, and the high susceptibility to the Ca2+ channel antagonist, nicardipine. 4. Isoprenaline and noradrenaline increased the amplitude of inward currents evoked by depolarizing pulses. The maximum inward current was potentiated by 43 .+-. 7% (n = 12) by isoprenaline and 39 .+-. 10% by noradrenaline (n = 6) at a concentration of 1 .mu.M. These effects were strongly inhibited by propranolol, but not phentolamine. Forskolin (10 .mu.M) also potentiated the currents to a similar degree. 5 It is suggested that stimulation of .beta.-adrenoceptors increases the amplitude of inward current through L-type Ca2+ channels in the pig coronary artery and that intracellular cyclic adenosine monophosphate is likely to be involved in this action.