Ko Eun A, Park Won Sun, Son Youn Kyoung, Kim Do Hyung, Kim Nari, Kim Hyoung Kyu, Choi Tae-Hoon, Jung In Duk, Park Yeong-Min, Han Jin
National Research Laboratory for Mitochondrial Signaling, FIRST Mitochondria Research Group, Department of Physiology and Biophysics, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan, Republic of Korea.
Vascul Pharmacol. 2009 Jan-Feb;50(1-2):51-6. doi: 10.1016/j.vph.2008.09.004. Epub 2008 Oct 11.
We examined the effect of the protein tyrosine kinase (PTK) inhibitor, genistein on voltage-dependent K+ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells, using whole-cell patch clamp techniques. The amplitude of the Kv current was inhibited by genistein in a dose-dependent manner, with a Kd value of 7.51 microM. Genistein had no effect on the steady-state activation or inactivation of Kv channels. The applications of trains of pulses at 1 or 2 Hz caused a progressive increase in the genistein-blockade. Genistein produced use-dependent inhibition of the Kv currents, consistent with a slow recovery from inactivation in the presence of genistein. Daidzein and genistin, two inactive analogs of genistein, showed an inhibitory effect similar to that of genistein on Kv channels. Moreover, the absence of ATP inside the pipette did not influence the blocking effect of genistein. We suggest that genistein directly inhibited the Kv current, independently of PTK inhibition.
