Aims: 

We finalized our previous study regarding the involvement of L-type calcium channels (Ca_L) in the constriction of human umbilical vessels, with reference to the umbilical artery and the action of angiotensin II and serotonin, also investigating the participation of store-operated calcium channels (capacitative calcium influx).

Methods: 

The 2 mm wide arterial rings were mechanically de-endothelised and equilibrated for 2 h under a resting tension of 2 g. The contraction force was normalised (%) to the contraction induced in the same ring by K ⁺ 80 mM (mean ± SEM; n = 4).

Results: 

We constructed dose-contraction curves for angiotensin II and serotonin in rings precontracted by 80 mM K⁺ (complete activation of the contractile mechanism based on depolarization and CaL). Separately we obtained dose-relaxation curves for the Ca_L blocker D600, in rings precontracted by serotonin 0.01 mM and angiotensin II 0.001 mM. The residual contraction after D600 10^-4 M was in both cases completely relaxed by blocking the calcium influx via store-operated channels (NiCl₂ 1 mM or 2-aminoetoxi-diphenylborane 0.1 mM).

Conclusion: 

This is the first study devoted to the pathways that ensure calcium influx for constriction of human umbilical arteries. The physiological relevance is discussed in comparison with the few data available in animal umbilical arteries and with reference to some classical aspects observed in other arterial preparations.

*CNCSIS grant interdisciplinary platform /68