THE EFFECTS OF HALOTHANE ON ARGININE-VASOPRESSIN-INDUCED CA2-MEDIATEDCA2+ ENTRY FROM THE EXTRACELLULAR-SPACE IN SINGLE CULTURED SMOOTH-MUSCLE CELLS OF RAT AORTA( MOBILIZATION FROM THE INTRACELLULAR STORES ANDTHE RECEPTOR)

Halothane has a direct action on vascular smooth muscle cells and caus es relaxation of these cells, yet neither the mechanism nor the site o f its action is completely understood. Using digital imaging microscop y with the Ca2+ indicator fura-2, the effects of halothane on the intr acellular [Ca2+] dynamics induced by arginine vasopressin (AVP) in the perinuclear region and cytosol in single cultured smooth muscle cells of rat aorta were studied. Changes in intracellular [Ca2+] were expre ssed as percent increases in the ratios of fluorescence intensity at 5 00 nm excited by 340 nm and 380 nm. AVP (10(-7) M) elicited an initial transient increase in [Ca2+] in the perinuclear region higher than th at in the cytosol in Ca2+-containing solution (346% +/- 21% and 213% /- 22%, respectively). Halothane, 0.5%, attenuated the [Ca2+] increase induced by AVP in the perinuclear region and cytosol, and halothane, 1.0% and 2.0%, abolished the differential increase. Under the continuo us application of AVP (10(-7) M), Ca2+ restoration in the medium after perfusion with Ca2+-free solution increased the perinuclear [Ca2+] mo re than the cytosolic [Ca2+]. Both were significantly attenuated by 2. 0% halothane, but not by nicardipine (10(-5) M) or ryanodine (10(-6) M ). Our results suggest that halothane may attenuate the Ca2+ release f rom the intracellular Ca2+ stores more than the receptor-mediated Ca2 entry from the extracellular space in the AVP-induced response in the se cells.