The Effects of Ketamine on Ca2+ Movements in A7r5 Vascular Smooth Muscle Cells

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Abstract
To investigate the effects of ketamine on Ca2+ movement to and from intracellular Ca2+ stores and across plasma membranes,45 Ca2+ fluxes were studied in permeabilized and intact A7r5 smooth muscle cells, an established cell line derived from embryonic rat aorta.Monolayers of A7r5 cells were loaded with45 Ca2+, and the radioactivity in the collected medium and the residual activity were measured by liquid scintillation counting. Ketamine had no effect on45 Ca2+ uptake and passive leak of the nonmitochondrial Ca2+ pool in permeabilized A7r5 cells. Ketamine 1 mM had no inhibitory effect on the inositol 1,4,5-trisphosphate (InsP3, 1 micro M)-induced Ca2+ release from the intracellular stores. In intact A7r5 cells, ketamine did not alter the Ca2+ extrusion from these cells under resting conditions. Addition of 10 nM vasopressin resulted in a transient Ca (2+) release from the intracellular stores. Ketamine inhibited this vasopressin-induced Ca2+ release, but did not enhance Ca2+ extrusion through the plasma membrane in the period after the vasopressin effect. These results indicate that ketamine inhibits agonist-induced Ca2+ release from intracellular stores, but has no effect on Ca2+-uptake into intracellular stores or on Ca2+ extrusion through the plasma membrane in A7r5 smooth muscle cells. (Anesth Analg 1996;83:1105-9)