Impairment and restoration of rat urinary bladder responsiveness following distension.

Micturition and bladder responsiveness in vitro were impaired in rats fed isotonic sucrose, afflicted with diabetes mellitus or diabetes insipidus. Their urinary output which was seven times control, initiated micturition responses at volumes three times control. Nerve-induced contractions by bladders from these rats developed substantially less pressure than control. Contractions elicited at 1 Hz by control and impaired bladders were potentiated equally by tetraethylammonium chloride (TEA) (5 mM) or by carbachol (2 X 10(-7) M). Contractions elicited at 20 Hz by normal bladders were not potentiated, those by impaired bladders were. TEA, by increasing transmitter release, and carbachol, by a postjunctional action, substantially reversed bladder dysfunction. Because control and impaired bladders were equally enhanced by TEA, prejunctional and contractile element (CE) activity at 1 Hz were probably unaffected by distension. However, postjunctional sensitivity was probably reduced. Impaired bladders, more compliant than controls, became less compliant after carbachol without elevating resting pressure. Whereas the action of carbachol to enhance bladder responsiveness did not involve tension development, there may have been cholinoceptor facilitation and shortening of CE.