Comparison of urinary bladder function in rats with hereditary diabetes insipidus, streptozotocin-induced diabetes mellitus, and nondiabetic osmotic diuresis.
In vivo and in vitro bladder function were studied in three different models of increased diuresis: 1) Brattleboro rats with hereditary diabetes insipidus (di/di), 2) Sprague-Dawley rats with streptozotocin-induced diabetes mellitus (STZ), and 3) Sprague-Dawley rats with increased diuresis due to 5% sucrose added to the drinking water. When compared with controls, all three models showed bladder mass, increased water consumption and urine output, higher mean and maximal increased micturition volumes, and greater bladder capacity and compliance by in vitro cystometry. The changes were more extensive in di/di rats than in the STZ and sucrose-drinking rats. The concentration of bladder collagen decreased in all three rat models when compared with controls. However, the collagen concentration of STZ bladders was significantly lower than the collagen concentration of di/di and sucrose bladders, suggesting that the decrease in bladder collagen concentration associated with experimental diabetes mellitus is only partly related to the increased diuresis. Contractile function was studied using a whole bladder model. Responses of whole bladders from control and diabetic rats to electrical field stimulation, carbachol and KCl were identical. Volume-pressure relations of the isolated whole bladder showed that the magnitude of the contractile response to KCl is constant at intravesical volumes ranging from about 10 to 95% of cytometrical bladder capacity. Bladders from Brattleboro di/di rats and STZ rats showed a rightward shift of volume-passive pressure curves when compared with appropriate controls. Bladders from sucrose-drinking rats had volume-passive pressure curves similar to the bladders from controls. This study suggests that while contractile function remains intact with increased diuresis, the passive function changes, with the bladder becoming more distensible.
Eika
B
B
Division of Urology, University of Pennsylvania School of Medicine, Philadelphia.
Levin
R M
RM
Longhurst
P A
PA
D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D003094:Collagen / Q000032:analysis; D003919:Diabetes Insipidus / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D004231:Diuresis / Q000502:physiology*; D004558:Electric Stimulation; D066298:In Vitro Techniques; D008365:Manometry; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009130:Muscle, Smooth / Q000187:drug effects / Q000502:physiology; D009994:Osmolar Concentration; D051381:Rats; D011910:Rats, Brattleboro; D017207:Rats, Sprague-Dawley; D001743:Urinary Bladder / Q000737:chemistry / Q000503:physiopathology*; D014554:Urination / Q000502:physiology
D002217:Carbachol; D003094:Collagen