AJP - Regulatory, Integrative and Comparative Physiology, Vol 244, Issue 1 106-R113, Copyright © 1983 by American Physiological Society
Impairment and restoration of rat urinary bladder responsiveness following distension
F. G. Carpenter
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.
