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Chloroquine, an Activator of Bitter Taste Receptors, Relaxed Male Guinea Pig Gallbladder Strips

Taste receptor cells are present in several extra‐oral locations such as the gut, human airway smooth muscle, vascular smooth muscle, and myometrial smooth muscle. A pharmacologic approach was used. The purpose of this study was to determine if the motility of the gallbladder was affected by a bitter tastant such as chloroquine (ChQ). ChQ relaxed both cholecystokinin octapeptide (CCK)‐ and KCl‐induced tension in a concentration dependent manner. There was no significant difference in the amount of ChQ‐induced relaxation of either CCK (1.0 nM) ‐ or KCl (40 mM)‐induced tension at any concentration of ChQ used (50, 100, 150, and 200 mM). In some strips ChQ induced a transient tension (0.4 g lasting 1.4min). To determine if ChQ inhibited extracellular Ca2+ entry, ChQ was added to the chambers prior to the CCK a significant decrease in the amount of CCK‐induced tension was observed (1.12±0.08 vs. 0.9±0.06 g, n=4, p<0.001). A similar result was observed when KCl was used (1.12±0.1 vs. 0.7±0.1 g, n=4, p<0.001). Penitrem A, a blocker of high conductance Ca2+ activated K+ channels, decreased the amount of ChQ‐induced relaxation (34.5±4.3 vs. 27.0±3.2%, n=3, p<0.02). Bisindolylmaleimide IV (BIM) and chelerythrine Cl− were used together to block PKC. They significantly decreased the amount of ChQ‐induced relaxation (23.8±3.2 vs. 18.9±3.0%, n=3, p<0.03). Neither PKA‐IM, a PKA blocker, nor KT5823, a PKG blocker, had a significant effect on the amount of ChQ‐induced relaxation. ChQ relaxed guinea pig gallbladder strips by blocking extracellular Ca2+ entry and blocked the actions of PKC.