Abstract

Diabetic lower urinary tract disfunction is well known, however, precise mechanism of the lower urinary tract disfunction remains to be solved. The present study is to clarify the lower urinary tract disfunction of diabetic rats by simultaneously measuring bladder and urethral pressures. Female wistar rats were administered with streptozotocin (STZ 65 mg/kg, i.p.) to induce diabetes mellitus. Bladder and urethral pressures during rhythmic bladder contractions were compared under urethane anesthesia (1.0 g/kg, i.v.) between the control rats, diabetic rats, and diuretic rats. The bladder contraction pressures of diabetic rats were decreased initially, but returned to the control values at 8 weeks. Atropine (2.5 mg/kg, i.a.) produced a marked reduction of bladder contraction pressure in the 8 weeks diabetic rats. The diabetic rats showed an increase of urethral pressure simultaneously with an increase of bladder pressure in the initial phase of rhythmic bladder contraction which is totally blocked by striated muscle relaxant. This phenomenon was not observed in the control or diuretic rats. Both group showed an initial decrease of urethral pressure followed by bladder contraction and rhythmic contractions of the urethra. Our results suggest that bladder muscarinic receptors of the 8 weeks diabetic rats are more dominant than those of the other groups, and Mahoney's 4th reflex (urethrosphincteric guarding reflex) is facilitated but Mahoney's 6th reflex (detruthodetrusor facilitative reflex) is suppressed in the diabetic rats. We think that in the diabetic rats, sensory inputs by bladder distension were weak and could not induce Mahoney's 6th reflex until certain threshold values. Diabetic rats might develop changes in the mode of spinal neuronal transmission.

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