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The systematic study of aging change of micturition.

排尿老化变化的系统研究。

基本信息

批准号：
10671465
负责人：
ISHIZUKA Osamu
金额：
$ 1.92万
依托单位：
Shinshu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

项目摘要

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.

前列腺增生等膀胱出口梗阻已成为引起膀胱功能亢进的常见疾病。这种多动可能是由于排尿神经控制老化所致。膀胱出口梗阻大鼠膀胱反射机制和几个神经的变化，包括肥大的背根神经节神经元支配膀胱的促进。脊髓速激肽受体和肾上腺素能受体已被证明在正常大鼠和膀胱出口梗阻大鼠的排尿中起作用。在这项研究中，我们可以证明，在脊髓上水平，此类受体也可能参与排尿控制。结果提示脊髓上NK受体和肾上腺素能受体可能是治疗膀胱出口梗阻后膀胱过度活动的药物靶点，随着年龄的增长，排尿的神经控制发生变化，其机制不能仅用肾上腺素能和副交感神经控制来解释。5-HT受体广泛分布于中枢神经系统，包括参与控制排尿反射通路的几个区域。在正常清醒大鼠中，研究了侧脑室（i. c. v.）给药5-HT，5-HT 1A受体、5-HT 2受体、5-HT 3受体和5-HT 4受体的激动剂。结果提示，在脊髓上水平，5-HT（通过5-HT_（1A）、5-HT_（2）和5-HT_（4）受体）可增强膀胱充盈引起的排尿反射。这也意味着5-HT受体拮抗剂，作用于5-HT 1A，5-HT 2和5-HT 4受体，可以作为治疗膀胱过度活动的药物的靶点，应该进行探索。