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Life Sci ; 193: 207-213, 2018 Jan 15.
Article in English | MEDLINE | ID: mdl-29100756

ABSTRACT

AIMS: More than half of diabetic patients experience voiding disorder termed diabetic urinary bladder dysfunction (DBD). Here we have investigated how the alterations in transient receptor potential vanilloid 1 (TRPV1) ion channel expressed in bladder-innervating afferents may contribute to DBD pathogenesis. MAIN METHODS: The rat model of streptozotocin (STZ)-induced diabetes was used. The functional profile of TRPV1 in retrogradely labeled afferent, bladder-innervating dorsal root ganglia (DRG) neurons was examined using patch clamp. The level of TRPV1 transcripts in DRG was assessed with qRT-PCR. TRPV1-dependent component of detrusor smooth muscle (DSM) contractions was studied with muscle strip tensiometry. KEY FINDINGS: TRPV1-mediated current (ITRPV1) was increased in diabetic animals vs. controls by 42%. The expression of Trpv1 gene was found to be 63% higher in STZ-treated rats compared to controls, consistent with the respective electrophysiological data. Surprisingly, capsaicin-induced contractions of DSM were found to be 3-to-10-fold weaker in diabetic group depending on concentration of the agonist (100nM to 10µM). SIGNIFICANCE: Our findings suggest the dual role of TRPV1 in DBD. On the one hand, the increase of its functional expression may enhance micturition reflex arc functioning. On the other hand, at the local level, the decrease of TRPV1-dependent contractions may contribute to organ decompensation.


Subject(s)
TRPV Cation Channels/metabolism , Urinary Bladder/physiopathology , Animals , Capsaicin/pharmacology , Diabetes Mellitus, Experimental/metabolism , Disease Models, Animal , Ganglia, Spinal/drug effects , Male , Muscle Contraction/drug effects , Muscle, Smooth/drug effects , Neurons/drug effects , Patch-Clamp Techniques/methods , Rats , Rats, Wistar , Reflex/drug effects , Streptozocin/metabolism , TRPV Cation Channels/genetics , Urinary Bladder/metabolism
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