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The actions of caffeine and 2,3‐butanedione monoxime on calcium transients in human vascular smooth muscle

Ca2+ mobilization by membrane depolarization or histamine application, was measured in isolated human uterine artery smooth muscle cells. Nifedipine, a Ca2+ channel blocker, was found to inhibit the depolarization‐induced increase in [Ca2+]i but not the histamine‐induced increase. This suggests the presence of functional voltage‐dependent Ca2+ channels and agonist‐induced mobilization of Ca2+ via a different mechanism. Caffeine inhibited both the depolarization‐ and histamine‐induced increases in intracellular calcium. The mechanisms of inhibition do not involve cAMP and point to a complex action of caffeine at multiple sites. The dephosphorylating agent 2,3‐butanedione monoxime (BDM) was found to block voltage‐dependent Ca2+ changes but not agonist‐induced changes suggesting a role for phosphorylation in the regulation of the Ca2+ channels in these cells.