Investigation into vanadate-induced potentiation of smooth muscle contractility in the rabbit isolated ileum.

The action of sodium orthovanadate (Na3VO4) on spontaneous mechanical activity of the longitudinal muscle was investigated in isolated segments of rabbit distal ileum. Vanadate (0.3-1000 microM) concentration-dependently enhanced the amplitude of phasic contractions (pendular movements) and caused the muscle tone to slightly increase at the highest concentrations. Both these effects were mimicked by the Ca2+ channel activator BAY K 8644 (10-1000 nM). Vanadate- and BAY K 8644-induced potentiation of mechanical activity was antagonized by the Ca2+ entry blocker nifedipine (3 nM). In Ca(2+)-free, K(+)-depolarized preparations, vanadate (100 microM) failed to contract the musculature, but potentiated the contractile response to applied calcium (CaCl2: 30-300 microM). The action of vanadate was similar to that of BAY K 8644 (3 nM) and was antagonized by nifedipine (0.1 nM). These results suggest that extracellular calcium is required for vanadate-induced smooth muscle excitation which, at least in part, appears to arise from facilitation of calcium influx through voltage-dependent Ca2+ channels.