Y. Kanmura et al., THE EFFECTS OF KETAMINE ON CA2-MUSCLE CELLS( MOVEMENTS IN A7R5 VASCULAR SMOOTH), Anesthesia and analgesia, 83(5), 1996, pp. 1105-1109
To investigate the effects of ketamine on Ca2+ movement to and from in
tracellular Ca2+ stores and across plasma membranes, Ca-45(2+) 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 with Ca-45(2+), and the radioactivity in the co
llected medium and the residual activity were measured by liquid scint
illation counting. Ketamine had no effect on Ca-45(2+) uptake and pass
ive leak of the nonmitochondrial Ca2+ pool in permeabilized A7r5 cells
. Ketamine 1 mM had no inhibitory effect on the inositol 1,4,5-trispho
sphate (InsP(3), 1 mu M)-induced Ca2+ release from the intracellular s
tores. In intact A7r5 cells, ketamine did not alter the Ca2+ extrusion
from these cells under resting conditions. Addition of 10 nM vasopres
sin resulted in a transient Ca2+ release from the intracellular stores
. Ketamine inhibited this vasopressin-induced Ca2+ release, but did no
t enhance Ca2+ extrusion through the plasma membrane in the period aft
er the vasopressin effect. These results indicate that ketamine inhibi
ts agonist-induced Ca2+ release from intracellular stores, but has no
effect on Ca2+-uptake into intracellular stores or on Ca2+ extrusion t
hrough the plasma membrane in A7r5 smooth muscle cells.