[The role of intra- and extracellular Ca in the activation of contraction of pulmonary artery smooth muscles induced by serotonin].

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.