Neural Control of Substance P Induced Up-Regulation and Release of Macrophage Migration Inhibitory Factor in the Rat Bladder. Export

@article{citeulike:2831031, abstract = {PURPOSE: Macrophage migration inhibitory factor is increased in intraluminal fluid after experimental inflammation and it mediates proinflammatory effects on the bladder. We examined the contribution of nerve activity and specific neurotransmitter systems to the mechanism of macrophage migration inhibitory factor release from the bladder during inflammation. MATERIALS AND METHODS: Male Sprague-Dawley rats were anesthetized. The bladders were emptied and filled with saline. Rats received saline as a control (0.1 ml/100 gm body weight) or substance P (Sigma(R)) (40 mug/kg in saline, 0.1 ml/100 gm body weight) subcutaneously as well as hexamethonium (Sigma) (50 mg/kg) intraperitoneally in saline (0.1 ml/100 gm body weight), lidocaine (2\%, 0.3 ml) intravesically, atropine (Sigma) (3 mg/kg in saline, 0.1 ml/100 gm body weight) intravenously, propranolol (Sigma) (3 mg/kg in saline, 0.1 ml/100 gm body weight) intravenously or phentolamine (Sigma) (10 mg/kg in saline, 0.1 ml/100 gm body weight) intravenously. After 1 hour the intravesical fluid was removed and the bladder was excised. Macrophage migration inhibitory factor levels in intraluminal fluid were measured by enzyme-linked immunosorbent assay and Western blotting. MIF expression in bladder homogenates was examined using reverse transcriptase-polymerase chain reaction. RESULTS: Intravesical lidocaine or ganglionic blockage with hexamethonium prevented substance P induced macrophage migration inhibitory factor release. In addition, pretreatment with atropine and phentolamine but not propranolol also prevented macrophage migration inhibitory factor release. While MIF up-regulation in the bladder was increased with substance P treatment, it was only prevented by intravesical lidocaine. CONCLUSIONS: Substance P induced macrophage migration inhibitory factor release in the bladder is mediated through nerve activation. Postganglionic parasympathetic (via muscarinic receptors) and sympathetic (via alpha-adrenergic receptors) fibers mediate macrophage migration inhibitory factor release, while activating bladder afferent nerve terminals up-regulates MIF.}, address = {Bay Pines Veterans Affairs Healthcare System, Research and Development, Bay Pines and Department of Surgery, University of South Florida, Tampa, Florida.}, author = {Vera, Pedro L L. and Wang, Xihai and Meyer-Siegler, Katherine L L.}, citeulike-article-id = {2831031}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.juro.2008.02.040}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/18499160}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=18499160}, day = {20}, doi = {10.1016/j.juro.2008.02.040}, issn = {1527-3792}, journal = {The Journal of urology}, keywords = {macrophage, mif, substance\_p}, month = {May}, posted-at = {2008-05-25 18:09:35}, priority = {2}, title = {Neural Control of Substance P Induced Up-Regulation and Release of Macrophage Migration Inhibitory Factor in the Rat Bladder.}, url = {http://dx.doi.org/10.1016/j.juro.2008.02.040}, year = {2008} }

TY - JOUR ID - citeulike:2831031 L3 - citeulike-article-id:2831031 N2 - PURPOSE: Macrophage migration inhibitory factor is increased in intraluminal fluid after experimental inflammation and it mediates proinflammatory effects on the bladder. We examined the contribution of nerve activity and specific neurotransmitter systems to the mechanism of macrophage migration inhibitory factor release from the bladder during inflammation. MATERIALS AND METHODS: Male Sprague-Dawley rats were anesthetized. The bladders were emptied and filled with saline. Rats received saline as a control (0.1 ml/100 gm body weight) or substance P (Sigma(R)) (40 mug/kg in saline, 0.1 ml/100 gm body weight) subcutaneously as well as hexamethonium (Sigma) (50 mg/kg) intraperitoneally in saline (0.1 ml/100 gm body weight), lidocaine (2%, 0.3 ml) intravesically, atropine (Sigma) (3 mg/kg in saline, 0.1 ml/100 gm body weight) intravenously, propranolol (Sigma) (3 mg/kg in saline, 0.1 ml/100 gm body weight) intravenously or phentolamine (Sigma) (10 mg/kg in saline, 0.1 ml/100 gm body weight) intravenously. After 1 hour the intravesical fluid was removed and the bladder was excised. Macrophage migration inhibitory factor levels in intraluminal fluid were measured by enzyme-linked immunosorbent assay and Western blotting. MIF expression in bladder homogenates was examined using reverse transcriptase-polymerase chain reaction. RESULTS: Intravesical lidocaine or ganglionic blockage with hexamethonium prevented substance P induced macrophage migration inhibitory factor release. In addition, pretreatment with atropine and phentolamine but not propranolol also prevented macrophage migration inhibitory factor release. While MIF up-regulation in the bladder was increased with substance P treatment, it was only prevented by intravesical lidocaine. CONCLUSIONS: Substance P induced macrophage migration inhibitory factor release in the bladder is mediated through nerve activation. Postganglionic parasympathetic (via muscarinic receptors) and sympathetic (via alpha-adrenergic receptors) fibers mediate macrophage migration inhibitory factor release, while activating bladder afferent nerve terminals up-regulates MIF. JF - The Journal of urology SN - 1527-3792 AD - Bay Pines Veterans Affairs Healthcare System, Research and Development, Bay Pines and Department of Surgery, University of South Florida, Tampa, Florida. TI - Neural Control of Substance P Induced Up-Regulation and Release of Macrophage Migration Inhibitory Factor in the Rat Bladder. KW - macrophage KW - mif KW - substance_p AU - Vera, Pedro L AU - Wang, Xihai AU - Meyer-Siegler, Katherine L PY - 2008/05/20/ UR - http://dx.doi.org/10.1016/j.juro.2008.02.040 ER -