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.