The systematic study of aging change of micturition.

膀胱出口梗阻，如良性前列腺肥大，正成为引起膀胱过度活动的常见病。这种多动症可能是排尿神经控制功能老化的结果。膀胱出口梗阻的大鼠表现出膀胱反射机制的易化和一些神经变化，包括支配膀胱的背根神经节神经元肥大。脊髓速激肽受体和肾上腺素能受体已被证明对正常大鼠和膀胱出口梗阻大鼠的排尿起作用。在这项研究中，我们可以证明，在脊髓上水平，这种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消除膀胱出口梗阻所致膀胱过度活动的药物靶点。随着年龄的增长，排尿的神经控制改变，其机制不能仅用肾上腺素和副交感神经控制来解释。5-羟色胺受体广泛分布于中枢神经系统，包括几个参与控制排尿反射通路的区域。我们在正常清醒大鼠中研究了其对脑室内膀胱测速图(i.c.v.)的影响。给予5-HT1受体、5-HT2受体、5-HT3受体和5-HT4受体激动剂5-羟色胺。结果提示，在脊髓上水平，5-羟色胺(通过5-HT1a、5-HT2和5-HT4受体)可增强膀胱充盈引起的排尿反射。这也意味着，作用于5-HT1a、5-HT2和5-HT4受体的5-羟色胺受体拮抗剂可以成为治疗膀胱多动的药物的靶点。

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.