van Breemen C, Siegel B
Circ Res. 1980 Mar;46(3):426-9. doi: 10.1161/01.res.46.3.426.
Norepinephrine (NE) activates isolated coronary conduit arteries by stimulating Ca2+ uptake into the smooth muscle cells. Blockade of Ca2+ influx by removal of Ca2+ from the bathing medium or addition of 10 mM LaCl3 prevents the NE-induced contraction in the dog coronary artery but still allows NE to induce a rapid transient contraction in the rabbit aorta. Under these conditions, NE stimulates 45Ca2+ efflux from rabbit aorta but fails to do so in the coronary artery. The difference in behaviour between the two arteries is attributed by the presence of an intracellular NE-sensitive Ca2+ fraction in the rabbit aorta and its absence from the dog coronary artery. This difference also explains the much greater sensitivity of the NE-induced contractions in the dog coronary to the relaxant effects of the Ca2+ antagonists, D600 and SKF525A, than that seen in the rabbit aorta. High K+-induced contractions of both the coronary artery and the aorta are equally sensitive to the Ca2+ antagonists.
去甲肾上腺素(NE)通过刺激平滑肌细胞摄取Ca2+来激活离体冠状动脉。通过从浴液中去除Ca2+或添加10 mM LaCl3来阻断Ca2+内流,可防止NE诱导的犬冠状动脉收缩,但仍允许NE诱导兔主动脉快速短暂收缩。在这些条件下,NE刺激兔主动脉中45Ca2+外流,但在冠状动脉中则无此作用。两条动脉行为的差异归因于兔主动脉中存在细胞内NE敏感的Ca2+部分,而犬冠状动脉中不存在。这种差异也解释了NE诱导的犬冠状动脉收缩对Ca2+拮抗剂D600和SKF525A的舒张作用的敏感性远高于兔主动脉。高钾诱导的冠状动脉和主动脉收缩对Ca2+拮抗剂同样敏感。