Abstract
The effect of carbachol on urinary acidification by the turtle bladder in vitro was studied. Carbachol inhibited urinary acidification in a dose-dependent fashion, with half maximal inhibition occurring at 4.5 x 10(-5) M. The effect of carbachol on urinary acidification could be totally prevented by atropine, indicating that the inhibition is mediated through a muscarinic receptor. Carbachol inhibited hydrogen ion secretion by decreasing the active proton conductance and not by altering the proton motive force. Carbachol failed to increase passive loss of hydrogen ion from the mucosa. Carbachol increased calcium uptake by the turtle bladder; this increase in calcium uptake could be prevented by pretreatment with atropine, pentobarbital, or lanthanum. Pentobarbital or lanthanum blunted the inhibitory effect of carbachol on hydrogen ion secretion. In the presence of low extracellular calcium (0.2 mM), carbachol failed to increase calcium uptake but caused a significant inhibition of hydrogen ion secretion. In the presence of normal calcium concentration, carbachol caused a significant efflux of calcium. These data demonstrate that carbachol inhibits urinary acidification and suggest that the mechanism of this inhibition may be related, at least in part, to changes in cytosolic calcium.
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