Voltage-gated sodium channels (Na_v) are responsible for the initiation and propagation of action potential in excitable cells. In vascular smooth muscle cells (VSMCs), usually electrically quiescent, their presence and functional impact are less well-defined, especially in human arteries.

In the present study, we determined Na_v channels gene expression profile and assessed the effect of Na_v channel activator veratridine on human arteries.

Human uterine arteries obtained from women undergoing hysterectomy were used. I_Na currents were electrophysiologically recorded on isolated VSMCs. Isometric tensions were recorded ex vivo on uterine artery rings in response to Na_v channel agonist (veratridine) and antagonist (tetrodotoxin, TTX) under physiological and hypoxic conditions.

A TTX-sensitive and fast inactivating I_Na current was recorded in VSCMs isolated from human uterine artery. Various Na_v channel genes were detected, corresponding to TTX-sensitive (Na_v1.2; 1.3; 1.7) and TTX-resistant (Na_v 1.5) alpha-subunit isoforms. Under hypoxic conditions, promotion of Na_v channel activity by veratridine triggered rhythmic oscillations in vascular tone of uterine arterial rings similar to vasomotion. This rhythmic activity was abolished by TTX (1 to 0.01μM) and attenuated by the calcium antagonist nifedipine (1μM).

Na_v channel are present in VSMCs of human arteries where they are functionally coupled to contractile activity. Under hypoxic condition, they could initiate, ex vivo, rhythmic contractile activity reminiscent of vasomotion. This is the first demonstration of Na_v channels contribution to this complex phenomenon.