KCNQ potassium channel expression in the caprine ureter and inhibition ofthecontractility of isolated distal caprine ureter by KCNQ channel opener Retigabine

Abstract

Voltage gated potassium channels i.eKCNQ potassium channels are expressed in several types of smooth muscles and may possibly mediate physiological responses in the tissues where they are expressed. Flupirtineand Retigabine is two smooth muscle relaxant agents that act by opening KCNQ (Kv7) potassium channels. This study was conducted to ascertain the ability of retigabine to inhibit the bethanechol inducedcontractility of isolated distal caprine (goat) ureter.The study suggests the presence of KCNQ potassium channels in the isolated caprine ureter based on the results obtained.The ability of 5,10,50, and 100µM concentrations of retigabine to inhibit the bethanechol induced contractility of isolated distal goat ureter was studied. The ability of the non-specific potassium channel blocker 4-aminopyridine (1mM) and the specific KCNQ channel blocker Linopirdinedihydrochloride (50 µM) to reverse the inhibitory effect of retigabine on ureteric contractility was also evaluated. The presence of KCNQ channels in isolated goat ureter was investigated using immunofluorescent microscopy.At the concentrations of 10, 50and 100µM concentrations, retigabine significantly inhibited the spontaneous contractility of the isolated goat ureter.At 10 µM Retigabineshowed a reduction of 19.2 % for a contact period of 10 minutes .The inhibitory effect ofretigabine on ureteric contractility was significantly reversed by 4-aminipyridine and Linopirdine.Immunofluorescent microscopy revealed the presence of KCNQ channels in the goat ureter.Retigabine inhibits the spontaneous contractility of the isolated goat ureter by opening KCNQ channels. Our study presents evidence of KCNQ channel expression in the goat ureter.

Keywords: Contractility, retigabine, isolated, KCNQ channel, ureter