大鼠主动脉中受体操纵性和电压门控性钙通道的药理学特性
Pharmacological characteristics of receptor-operated and potential-operated Ca2+ channels in rat aorta.
作者信息
Chiu A T, McCall D E, Timmermans P B
出版信息
Eur J Pharmacol. 1986 Aug 7;127(1-2):1-8. doi: 10.1016/0014-2999(86)90199-8.
In the rat aorta activation of the potential-operated Ca2+ channels by 100 mM K+ resulted in a greater 45Ca2+ influx than stimulation of the receptor-operated Ca2+ channels by norepinephrine (NE, 3 X 10(-7) M) or angiotensin II (AII, 10(-7) M). 45Ca2+ influx induced by NE was inhibited by prazosin (10(-7) M) but not by yohimbine (10(-6) M) while that by AII was abolished by [Sar1, Ile8]AII (10(-8) M). These receptor antagonists had no effect on the 45Ca2+ influx produced by K+. Bay k 8644 enhanced the influxes to low concentrations of NE and K+ while it was additive with the maximal concentration of NE but not with K+. 3-Isobutyl-1-methyl-xanthine and forskolin inhibited both the influx and efflux of 45Ca2+ elicited by NE but were ineffective against those caused by K+. Nifedipine blocked the efflux of 45Ca2+ induced by K+ but not that evoked by NE. However, both types of Ca2+ channel exhibited the same sensitivity to inhibition by Ca2+ entry blockers (nifedipine/verapamil) on 45Ca2+ influxes. These data suggest that in the rat aorta, the receptor-operated calcium channels and potential-operated calcium channels share similar structural characteristics. However, they are gated separately and distinctly by their respective activators.
在大鼠主动脉中，100 mM K⁺对电压门控性Ca²⁺通道的激活所导致的⁴⁵Ca²⁺内流，比去甲肾上腺素（NE，3×10⁻⁷ M）或血管紧张素II（AII，10⁻⁷ M）对受体门控性Ca²⁺通道的刺激所引起的⁴⁵Ca²⁺内流更多。NE诱导的⁴⁵Ca²⁺内流被哌唑嗪（10⁻⁷ M）抑制，但不被育亨宾（10⁻⁶ M）抑制，而AII诱导的⁴⁵Ca²⁺内流则被[Sar¹, Ile⁸]AII（10⁻⁸ M）消除。这些受体拮抗剂对K⁺产生的⁴⁵Ca²⁺内流没有影响。Bay k 8644增强了低浓度NE和K⁺引起的内流，而它与NE的最大浓度呈相加作用，但与K⁺不是。3-异丁基-1-甲基黄嘌呤和福斯可林抑制了NE引起的⁴⁵Ca²⁺的内流和外流，但对K⁺引起的⁴⁵Ca²⁺的内流和外流无效。硝苯地平阻断了K⁺诱导的⁴⁵Ca²⁺外流，但不阻断NE引起的⁴⁵Ca²⁺外流。然而，两种类型的Ca²⁺通道对Ca²⁺内流阻滞剂（硝苯地平/维拉帕米）抑制⁴⁵Ca²⁺内流表现出相同的敏感性。这些数据表明，在大鼠主动脉中，受体门控性钙通道和电压门控性钙通道具有相似的结构特征。然而，它们由各自的激活剂分别且明显地控制门控。
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