Nerve growth factor release from the urothelium increases via activation of bladder C-fiber in rats with cerebral infarction.
OBJECTIVE
There are some reports that bladder C-fibers are partially involved in detrusor overactivity in patients with brain lesions. We investigated the contribution of bladder C-fiber to decreased bladder capacity in rats with cerebral infarction.


METHODS
Cerebral infarction was induced under halothane anesthesia by left middle cerebral artery occlusion with 4-0 nylon thread in female Sprague-Dawley rats. Intramural amounts of ATP and prostaglandin E2, in vivo and in vitro ATP, NGF, and prostaglandin E2release from the distended bladder urothelium, and changes in mRNA expressions of sensor molecules and receptors were monitored 6 h after the occlusion. Cystometry was performed in rats with or without resiniferatoxin pretreatment.


RESULTS
Overexpression of sensor molecule, transient receptor potential vanilloid-type channel 1, acid-sensing ion channel 2, purinergic receptors P2X3, and M2/M3muscarinic receptors was found in the bladder. These changes were accompanied by increases in ATP and NGF release from the urothelium. In contrast, when bladder C-fibers were desensitized by resiniferatoxin, no increase in NGF release from the urothelium was found either in vivo or in vitro. There was no difference in the percentage decrease in bladder capacity between cerebral infarction rats pretreated with resiniferatoxin and cerebral infarction rats without pretreatment.


CONCLUSIONS
Results indicate that expression of sensor molecules in the bladder is altered by distant infarction in the brain. ATP and NGF release from the urothelium also increased. NGF release was related to activation of bladder C-fibers. Bladder C-fibers might not contribute much to decreased bladder capacity caused by cerebral infarction.
Faculty of Medical Science, Department of Urology, University of Fukui, Fukui, Japan.
Ryusei
R
Yokokawa
Faculty of Medical Science, Department of Urology, University of Fukui, Fukui, Japan.
Hironobu
H
Akino
Faculty of Medical Science, Department of Urology, University of Fukui, Fukui, Japan.
Hideaki
H
Ito
Faculty of Medical Science, Department of Urology, University of Fukui, Fukui, Japan.
Xinmin
X
Zha
Faculty of Medical Science, Department of Urology, University of Fukui, Fukui, Japan.
Osamu
O
Yokoyama
D062565:Acid Sensing Ion Channels / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002544:Cerebral Infarction / Q000378:metabolism* / Q000503:physiopathology; D005260:Female; D009130:Muscle, Smooth / Q000378:metabolism* / Q000503:physiopathology; D036421:Nerve Fibers, Unmyelinated / Q000502:physiology*; D020932:Nerve Growth Factor / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D043585:Receptor, Muscarinic M2 / Q000378:metabolism; D043587:Receptor, Muscarinic M3 / Q000378:metabolism; D058477:Receptors, Purinergic P2X3 / Q000378:metabolism; D001743:Urinary Bladder / Q000294:innervation* / Q000378:metabolism; D053201:Urinary Bladder, Overactive / Q000378:metabolism / Q000503:physiopathology; D019459:Urothelium / Q000378:metabolism* / Q000503:physiopathology
D062565:Acid Sensing Ion Channels; D043585:Receptor, Muscarinic M2; D043587:Receptor, Muscarinic M3; D058477:Receptors, Purinergic P2X3; D000255:Adenosine Triphosphate; D020932:Nerve Growth Factor
C-fiber; cerebral infarction; nerve growth factor; urinary bladder; urothelium