Buryĭ V A, Gurkovskaia A V, Gokina N I, Shuba M F
Biull Eksp Biol Med. 1988 Sep;106(9):261-4.
In Ca-free EGTA-containing solution serotonin induced a transient contraction of rabbit pulmonary artery smooth muscle which decayed to nearly steady-state level accounted for 17.7 +/- 1.6% of original contraction in Krebs solution. Both phasic and tonic components of this contraction were effectively inhibited by verapamil and Cd2+. Caffeine induced no contraction of muscle strips if it was applied after withdrawal of serotonin. But when the sequence of these drugs application was reversed, serotonin still evoked contraction with reduced phasic component. The results obtained in these experiments suggest, that serotonin-induced contraction of pulmonary artery smooth muscle is partly (less than 20%) due to mobilization of bound calcium from at least two stores located on the opposite sides of the cell membrane. Calcium released from external store site enters the cell via receptor-operated calcium channels.
在不含钙的含乙二醇双四乙酸（EGTA）溶液中，血清素可引起兔肺动脉平滑肌的短暂收缩，该收缩衰减至接近稳态水平，此稳态水平占克雷布斯溶液中原始收缩的17.7±1.6%。维拉帕米和镉离子（Cd2+）可有效抑制该收缩的相性和紧张性成分。如果在撤出血清素后应用咖啡因，则不会引起肌条收缩。但是当这些药物的应用顺序颠倒时，血清素仍可引起收缩，但其相性成分减少。这些实验获得的结果表明，血清素诱导的肺动脉平滑肌收缩部分（小于20%）是由于从位于细胞膜两侧的至少两个储存部位动员结合钙所致。从外部储存部位释放的钙通过受体操纵性钙通道进入细胞。
