The possible involvement of basolateral K+ channels in the intestinal response to secretagogues was investigated using stripped sheets of rat mid-intestine. Increasing the serosal K+ concentration reduced the rise in short-circuit current induced by acetylcholine, 5-hydroxytryptamine, theophylline and prostaglandin E2 (PGE2) without affecting the change caused by glucose. The secretagogue-induced rise in short-circuit current was inhibited by quinine, but not by tetraethylammonium chloride, apamin or 3,4-diaminopyridine. Acetylcholine stimulated 86Rb efflux into the serosal fluid from pre-loaded intestinal sheets and a smaller response was observed with PGE2. The acetylcholine-induced stimulation of 86Rb efflux was inhibited by serosal quinine and lack of serosal Ca2+. Furosemide in the serosal fluid reduced the electrical response to acetylcholine without affecting the increase in 86Rb efflux. It is concluded that as well as increasing luminal Cl- permeability, intestinal secretagogues also enhance the basolateral K+ conductance by activating Ca2+-dependent K+ channels.
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