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 μM) 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 Ca2+-free, K+-depolarized preparations, vanadate (100 μM) failed to contract the musculature, but potentiated the contractile response to applied calcium (CaCl2: 30-300 μM). 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.
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