European urology supplements vol:5 issue:14 pages:799-799
INTRODUCTION & OBJECTIVES: It has been demonstrated that intravesical volume load increases amplitude and frequency of autonomous bladder contractions . Thus local afferent-efferent reflexes, free from spinal and central neuronal pathways, seem to be involved in stretch-contractile responses in bladder. However the mechanisms underlying these stretch-evoked reflexes are still poorly understood.
In the present study we looked at the role of the vanilloid transient receptor potential channel subtype-1 (TRPV1) in local stretch-evoked rat bladder contractility.
MATERIAL & METHODS: Wistar rat bladders were used. Each bladder was excised,a pressure catheter was inserted and the bladder preparation was placed in a heated organ bath, where intravesical pressures were measured. The effects on autonomous bladder contractility of intravesical volume load (Krebs solution, 20 ml/min, 15 min)and of the TRPV1 agonist piperine  (PIP, 10 mM) were studied. The effects
of extravesical pre-treatment with TRP-antagonist ruthenium red (RR, 10mM)) and TRPV1-antagonist capsazepine (CZP, 10mM) on the stretch-contractile response were studied. These contractile responses were compared with data from untreated bladders.
RESULTS: Intravesical volume load induced an increase in amplitude and frequency of autonomous bladder contractions. The TRPV1-agonist PIP provoked similar effects,which were effectively antagonized by CZP. CZP and RR induced a decreased rise in amplitude of contractions after intravesical volume load, compared with the control group (p<0,05). Intravesical volume load provoked an increase in duration of contractions in CZP-treated bladders (p<0,05), but not in RR-bladders or controls. Intravesical volume load induced a decrease in frequency of contractions in RR-treated bladders (p<0,05), but not in CZP-bladders or controls. The effects of volume load on baseline and on superimposed contractile activity were unaffected by CZP and RR
CONCLUSIONS: We found evidence for involvement of TRP-channels and TRPV1 in particular in stretch-contractile responses in isolated rat bladders. TRPV1 seems to act as a pressure-sensing molecule, necessary for evoking contractile responses on intravesical volume load. The pressure-contractile response can be modified in patients
with overactive bladder disease. Further research is needed to elucidate the role of TRPV1 in affected bladder sensing, and to look for possible therapeutical perspectives of interacting on TRPV1 in functional bladder disorders.