| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
Bladder outlet obstruction, such as benign prostatic hypertrophy, is becoming common disease which causes bladder hyperactivity. This hyperactivity may results from the aging of the nervous control of the micturition. Rats subjected to bladder outlet obstruction show facilitation of bladder reflex mechanisms and several neural changes, including hypertrophy of the dorsal root ganglionic neurons innervating the bladder. Spinal tachykinin receptors and adrenergic receptors have been shown to play a role for micturition, both in normal rats and rats with bladder outlet obstruction. In this study, we could demonstrated that, at the supraspinal level such receptors may also be involved in micturition control. The results implies that supraspinal NK receptors and adrenergic receptors are a possible target for drugs aimed for elimination of bladder hyperactivity secondary to bladder outlet obstruction.
By aging, the nervous control of micturition changes and the mechanism cannot be explained by only adrenergic and parasympathetic nervous control. 5-HT receptors are widely distributed in the central nervous system, including several areas involved in the control of micturition reflex pathways. We studied in normal conscious rats, the effects on the cystometrogram of intracerebroventricular (i.c.v.) administration of 5-HT, an agonist at 5-HT1A receptors, 5-HT2 receptors, 5HT3 receptors and 5-HT4 receptors. The results suggest that, at the supraspinal level, 5-HT (via 5-HT1A, 5-HT2 and 5-HT4 receptors) can enhance the micturition reflex induced by bladder filling. This also means that 5-HT receptor antagonists, acting at 5-HT1A, 5-HT2 and 5-HT4 receptors, can be targets for drugs meant for treatment of bladder hyperactivity, should be explored.
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