@article{oai:niigata-u.repo.nii.ac.jp:00019958, author = {冨士原, 秀善}, issue = {8}, journal = {新潟医学会雑誌, 新潟医学会雑誌}, month = {Aug}, note = {The effects of halothane on the spatial and temporal dynamics of intracellular Ca^<2+> concentration in single cultured smooth muscle cells of the rat aorta were studied by digital imaging microscopy using Ca^<2+> indicator fura-2. Changes in intracellular[Ca^<2+>]were expressed as the ratios of fluorescence intensity at 500 nm excited by 340 nm and 380 nm. Halothane (0.5, 1.0, 2.0vol. %) itself had no detectable basal [Ca^<2+>] changes in these cells. Arginine-vasopressin (AVP; 10^<-7>M), one of vasoconstrictor agonists which mobilize intracellular Ca^<2+> by inositol 1, 4, 5-trisphosphate-induced Ca^<2+> release mechanism, increased the nuclear [Ca^<2+>] more than the cytosolic [Ca^<2+>]. The increases in the nuclear [Ca^<2+>] induced by AVP were greatly reduced by pretreatment with caffeine and ryanodine which deplete the caffeine-ryanodine sensitive intracellular Ca^<2+> storage. Halothane (0.5, 1.0, 2.0%) greatly attenuated the increase in [Ca^<2+>] in both the nuclear and cytosolic regions. Halothane (1.0, 2.0%) abolished the differential rise in [Ca^<2+>]in both regions in response to AVP. The times to the peak responses of [Ca^<2+>] were significantly prolonged by halothane. The results suggest that nucleus and/or perinuclear region are important Ca^<2+> store sites in response to AVP, and also that the caffeine and ryanodine sensitive Ca^<2+> storage sites exist in the perinuclear region. The results further suggest that halothane affects arginine-vasopressin-induced [Ca^<2+>] increase by an inhibition of inositol 1, 4, 5-trisphosphate production and/or by an inhibition of inositol 1, 4, 5-trisphosphate-induced Ca^<2+> release from intracellular Ca^<2+> storage sites.}, pages = {728--737}, title = {アルギニンバゾプレッシンによる血管平滑筋細胞内カルシウムイオン濃度の分布に及ぼすハロセンの影響}, volume = {107}, year = {1993} }