Beta-adrenergic receptor-mediated calcium mobilization in the human Jurkat T cell line.
The regulation of Ca2+ mobilization by beta-adrenergic receptor in the human Jurkat T cell line was investigated. Jurkat cells had a single class of beta-adrenergic receptor binding sites. Isoproterenol (ISP) caused the increase in cytosolic free Ca2+ concentration ([Ca2+]i) in a dose-dependent manner. In the absence of extracellular Ca2+, the pretreatment with OKT3, an anti-CD3 antibody, did not affect a transient increase in [Ca2+]i induced by the subsequent addition of ISP, and vice versa. On the other hand, the pretreatment with thapsigargin abolished the response of [Ca2+]i to the subsequent additions of ISP and OKT3. In permeabilized Jurkat cells, the addition of cAMP released Ca2+ from the intracellular Ca2+ pool. Neither nimodipine nor H8, a protein kinase A inhibitor, affected the increase in [Ca2+]i induced by ISP. The results suggest that cAMP accumulated by the activation of beta-adrenergic receptor may directly release Ca2+ from the inositol trisphosphate-insensitive intracellular Ca2+ pool in Jurkat T cells.
Takemura
H
H
Department of Pharmacology, School of Medicine, Sapporo Medical University, Japan.
Hatta
S
S
Yamada
K
K
Ohshika
H
H
D002118:Calcium / Q000378:metabolism*; D002460:Cell Line; D000242:Cyclic AMP / Q000378:metabolism; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D004789:Enzyme Activation; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate / Q000494:pharmacology; D007424:Intracellular Fluid / Q000378:metabolism; D009553:Nimodipine / Q000494:pharmacology; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D012680:Sensitivity and Specificity; D013601:T-Lymphocytes / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure*
D011943:Receptors, Adrenergic, beta; D009553:Nimodipine; D015544:Inositol 1,4,5-Trisphosphate; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D002118:Calcium