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. Author manuscript; available in PMC: 2006 Jun 1.
Published in final edited form as: Am J Physiol Heart Circ Physiol. 2005 Jan 28;288(6):H2628–H2636. doi: 10.1152/ajpheart.00992.2004

Fig. 1.

Fig. 1

Genistein, a broad-spectrum protein tyrosine kinase (PTK) blocker, augmented swelling-activated Cl− current (ICl,swell). A: current-voltage (I-V) relationship in isosmotic (1T) solution, after swelling in hypoosmotic (0.7T) solution for 10 min, after exposure to 100 μM genistein in 0.7T solution for 10 min (Gen), and after addition of 10 μM tamoxifen (Tam), a selective ICl,swell blocker, to 0.7T plus genistein solution. I-V curves cross near the Cl− equilibrium potential (ECl), which is −42 mV. B: families of swelling-induced difference currents. ICl,swell partially inactivated at positive potentials. C: genistein-induced difference currents in 0.7T solution. D: tamoxifen-sensitive difference currents in 0.7T plus genistein solution. Swelling activated outwardly rectifying ICl,swell that reversed near ECl and was stimulated by genistein. Tamoxifen blocked both the swelling- and genistein-induced components. Calibrations apply to all current records.