Harder D R
Pflugers Arch. 1981 Jun;390(3):296-8. doi: 10.1007/BF00658280.
Intracellular membrane potential (EM) and force development were measured in rabbit basilar artery to help elucidate the mechanism of action of dopamine in this preparation. There was a strong correlation between membrane depolarization and contraction (r = 0.95) between 3 X 10-7 M to 10-4 M dopamine. When the vascular muscle cells were depolarized by elevating [K]0 there was a Em dependent decrease in force development in response to dopamine. Significant reduction of dopamine stimulated force development was observed when the vessel was depolarized by 5-6 mV by excess extracellular K+ and 90% inhibition was seen when the artery was depolarized to -20mV. When Ca++ influx was blocked, dopamine no longer induced force development. Such findings suggest that dopamine contracts rabbit basilar artery by a mechanism involving membrane depolarization. This process may involve an influx of extracellular Ca++ through voltage sensitive channels.
在兔基底动脉中测量细胞内膜电位（EM）和力的发展，以帮助阐明多巴胺在此制剂中的作用机制。在3×10⁻⁷ M至10⁻⁴ M多巴胺之间，膜去极化与收缩之间存在很强的相关性（r = 0.95）。当通过升高[K]₀使血管平滑肌细胞去极化时，对多巴胺的反应中力的发展存在Em依赖性降低。当血管被过量的细胞外K⁺去极化5 - 6 mV时，观察到多巴胺刺激的力发展显著降低，当动脉去极化至-20 mV时，可见90%的抑制。当Ca²⁺内流被阻断时，多巴胺不再诱导力的发展。这些发现表明，多巴胺通过涉及膜去极化的机制使兔基底动脉收缩。这个过程可能涉及细胞外Ca²⁺通过电压敏感通道的内流。
