The presence of ATP-regulated K+ (KATP) channels in Tenebrio molitor Malpighian tubules was investigated by examining the effect of glibenclamide on both fluid secretion and basolateral membrane potentials (Vbl). Glibenclamide, a KATP channel blocker, slowed fluid secretion of Tenebrio tubules. In low bath K+ concentration (5 mmol l-1), glibenclamide either hyperpolarized or depolarized Vbl, resembling the effect seen with Ba2+. Subsequent addition of 6 mmol l-1Ba2+ caused a further hyper- or depolarization of Vbl. In control Ringer (50 mmol l-1 KCl, 90 mmol l-1 NaCl), glibenclamide had no visible effect on Vbl. The effect of ouabain was investigated in low bath[K+] in the presence of Ba2+. Vblresponded by a small but significant hyperpolarization from -51±4 mV to-56±4 mV (n=16, P<0.001) in response to 1 mmol l-1 ouabain. Repeating the experiments in the presence of both glibenclamide and Ba2+ resulted in a depolarization of Vbl when ouabain was added. In low bath [K+](high Na+), the Na+/K+-ATPase is expected to function at a high rate. In the presence of Ba2+, replacing Na+ by K+ rapidly depolarized Vbl,but this was followed by a repolarization. Repeating the experiments in the presence of glibenclamide markedly reduced the depolarizing effect and abolished the repolarization, with a gradual decrease in the sensitivity of Vbl to the surrounding [K+]. These results suggest the presence of KATP channels in the basolateral membrane. Glibenclamide had no visible effect on Vbl in high K+ or in the absence of Ba2+, indicating that other highly conductive K+ channels may mask the effect on KATP channels. This is the first demonstration of the presence of KATP channels in an insect epithelium.

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