TY - JOUR T1 - Ca<sup>2+</sup> Influx through Nonselective Cation Channels Plays an Essential Role in Noradrenaline-Induced Arachidonic Acid Release in Chinese Hamster Ovary Cells Expressing α<sub>1A</sub>-, α<sub>1B</sub>-, or α<sub>1D</sub>-Adrenergic Receptors JF - Journal of Pharmacology and Experimental Therapeutics JO - J Pharmacol Exp Ther SP - 901 LP - 907 VL - 299 IS - 3 AU - Yoshifumi Kawanabe AU - Nobuo Hashimoto AU - Tomoh Masaki AU - Soichi Miwa Y1 - 2001/12/01 UR - http://jpet.aspetjournals.org/content/299/3/901.abstract N2 - We constructed Chinese hamster ovary (CHO) cells stably expressing α1A-, α1B-, or α1D-adrenergic receptors (CHO-α1A, CHO-α1B, or CHO-α1D, respectively) and compared the Ca2+channels activated by noradrenaline (NA) in these cells using whole-cell recordings and monitoring of the intracellular free Ca2+ concentration ([Ca2+]i). We also investigated the involvement of Ca2+ channels in the NA-induced arachidonic acid release. In all three cell types, NA at concentrations ≥10 nM induced a sustained increase in [Ca2+]i attributable to extracellular Ca2+ influx in [Ca2+]i monitoring and an inward current in whole-cell recording. The current-voltage relationships were linear, and their reversal potentials were close to 0 mV. The reversal potential of the currents was not affected by a change in the concentration of Cl− in the bath solution. Moreover, a current could be induced in a bath solution containing only Ca2+ as the movable cation. LOE 908, a receptor-operated Ca2+ channel blocker, inhibited the sustained increase in [Ca2+]i and inward currents in a concentration-dependent manner, and complete inhibition was observed at concentrations ≥ 3 μM. NA induced arachidonic acid release in all three cell types. This release was entirely dependent on extracellular Ca2+ influx. Moreover, LOE 908 at concentrations ≥ 3 μM blocked the NA-induced increase in arachidonic acid release. These results indicate that 1) NA activates LOE 908-sensitive Ca2+-permeable nonselective cation channels (NSCCs) in CHO-α1A, CHO-α1B, and CHO-α1D, and 2) the Ca2+ influx through NSCCs may play an important role in the NA-induced enhancement of arachidonic acid release in these cells. The American Society for Pharmacology and Experimental Therapeutics ER -