The effects of halothane on arginine-vasopressin-induced Ca2+ mobilization from the intracellular stores and the receptor-mediated Ca2+ entry from the extracellular space in single cultured smooth muscle cells of rat aorta.

Halothane has a direct action on vascular smooth muscle cells and causes relaxation of these cells, yet neither the mechanism nor the site of its action is completely understood. Using digital imaging microscopy with the Ca2+ indicator fura-2, the effects of halothane on the intracellular [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 expressed as percent increases in the ratios of fluorescence intensity at 500 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 that in the cytosol in Ca(2+)-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 continuous application of AVP (10(-7) M), Ca2+ restoration in the medium after perfusion with Ca(2+)-free solution increased the perinuclear [Ca2+] more 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 from the intracellular Ca2+ stores more than the receptor-mediated Ca2+ entry from the extracellular space in the AVP-induced response in these cells.