Changes in Cell Volume Induced by Activation of the Cyclic AMP-Dependent Chloride Channel in Guinea-Pig Cardiac Myocytes.

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Abstract

The effects of the activation of cyclic AMP–dependent Cl− current (ICl,cAMP) on cell volume were studied at various [K+]o under isosmotic conditions in guinea-pig ventricular myocytes. The area of the cell image obtained with videomicroscopy was used as an index of cell volume. ICl,cAMP was activated by adrenaline (5.5 μM). Measurements of the membrane potential (Vm) were performed by the gramicidin-perforated patch-clamp method. At 5.4 mM [K+]o with low [Cl−]o, where Vm was negative to the predicted equilibrium potential of Cl− (ECl), adrenaline sizably decreased the cell area. At high [K+]o with normal [Cl−]o, where Vm was positive to ECl, adrenaline increased the cell area; at 145.4 mM [K+]o the cell area was increased to 110% of control on average (n = 22). The cells swollen in this manner shrank when [Cl−]o was reduced to a low level in the presence of adrenaline. The results indicate that the induction of Cl− influxes (outward ICl,cAMP) or effluxes (inward ICl,cAMP) can lead to a cell swelling or shrinkage, respectively. The addition of BaCl2 (1 mm), a blocker of K+ channels, attenuated the adrenaline-dependent cell swelling, supporting the view that Cl− fluxes must be accompanied by cofluxes of K+ ions to affect the cell volume. The adrenaline-dependent cell swelling was inhibited by antagonizing β-adrenergic stimulation with acetylcholine or by blocking ICl,cAMP channels with glibenclamide, confirming the involvement of ICl,cAMP in the adrenaline response. The results show that the activation of ICl,cAMP can shrink or inflate the cardiac cells under isosmotic conditions, depending on Vm and ECl.<br>

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