Tachykinins as modulators of the micturition reflex in the central and peripheral nervous system

In the normal urinary bladder, tachykinins (TKs) are expressed in a populat ion of bladder nociceptors that is sensitive to the excitatory and desensit izing effects of capsaicin (i.e., capsaicin-sensitive primary afferent neur ons (CSPANs)). Several endobiotics or xenobiotics excite CSPANs and release TKs and other mediators at both the peripheral and spinal cord level. The peripheral release of TKs determines a set of responses (known as neurogeni c inflammation) that includes vasodilatation. plasma protein extravasation, smooth muscle contraction and stimulation of afferent nerves. Following ch ronic inflammation, both immune cells and capsaicin-resistant sensory neuro ns can de novo express TKs: whether these pools of TKs are releasable and c ontribute to inflammatory processes is presently unsettled. At the spinal c ord level. the release of TKs contributes in determining an altered pattern of vesicourethral reflexes in response to nociceptive stimulation of the b ladder by conveying: (a) the afferent transmission to supraspinal sites. an d (b) descending or sensory inputs to the sacral parasympathetic nucleus (S PN). Recent evidence also attribute a synergetic role of TKs in the suprasp inal modulation of the sensory arm of the micturition reflex. The overall available information suggests that TK receptor antagonists may affect bladder motility/reflexes which occur during different pathological states, while having little influence on the normal motor bladder function . (C) 2001 Elsevier Science B.V. All rights reserved.