Excitatory and inhibitory urinary bladder reflexes induced by stimulation of cervicovaginal capsaicin-sensitive sensory fibers in rats.
ABSTRACT We have investigated the effect of intravaginal application of capsaicin on micturition reflex in female rats. Urinary bladder contractility was measured by transurethral pressure recording at isovolumetric and subthreshold conditions in anaesthetized rats. The intravaginal application of capsaicin (15 microg/50 microl rat) induced reproducible bladder phasic contractions, without desensitization upon repeated applications, that were blocked by intravenous atropine (1 mg/kg) or hexamethonium (5 mg/kg) and prevented by removal of paracervical ganglia or systemic capsaicin pretreatment (125 mg/kg, s.c.). The inhibition of sympathetic transmission by guanethidine (30 mg/kg, s.c.) produced significant increase of the bladder reflex contractions activated by intravaginal capsaicin. Intravenous administration of the TRPV1 antagonist, capsazepine (3 mg/kg), significantly reduced the excitatory reflex response to capsaicin. Intravaginal administration of capsaicin (15 microg/50 microl), during distension-induced reflex bladder contractions, produced a transient block of reflexes, unaffected by guanethidine pretreatment. In conclusion, the stimulation of capsaicin-sensitive sensory nerve endings in the rat cervix-vagina induced a dual excitatory or inhibitory bladder response in anaesthetized female rats depending on the degree of bladder distension.
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ABSTRACT: The transient receptor potential vanilloid subfamily 1 (TRPV1) is an ion channel activated by capsaicin, heat, protons and endogenous ligands such as anandamide. It is largely expressed in the urinary tract of mammals. Structures in which the receptor expression is firmly established include sensory fibers and urothelial cells, although the presence of TRPV1 in other cell types has been reported. As in other systems, pain perception was the first role attributed to TRPV1 in the urinary tract. However, it is now increasingly clear that TRPV1 also regulates the frequency of bladder reflex contractions, either through direct excitation of sensory fibers or through urothelial-sensory fiber cross talk involving the release of neuromediators from the epithelial cells. In addition, the recent identification of the receptor in urothelial and prostatic cancer cells raise the exciting hypothesis that TRPV1 is involved in cell differentiation. Desensitization of the receptor by capsaicin and resiniferatoxin has been investigated for therapeutic purposes. For the moment, lower urinary tract dysfunctions in which some benefit was obtained include painful bladder syndrome and overactive bladder of neurogenic and non-neurogenic origin. However, desensitization may become obsolete when non-toxic, potent TRPV1 antagonists become available.Archiv für Experimentelle Pathologie und Pharmakologie 08/2006; 373(4):287-99. · 2.15 Impact Factor
- Journal of Autonomic Pharmacology 07/1986; 6(2):133-62.
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ABSTRACT: Afferent activity from the reproductive tract activates intrinsic pain attenuating processes. For example, analgesia results from vaginocervical mechano-stimulation in nonpregnant rats and occurs during pregnancy and parturition. In the present study, the effect of uterocervical mechanostimulation on pain thresholds was investigated in order to determine whether direct stimulation of the uterine cervix could play a role in the analgesia of pregnancy. Uterocervical mechanostimulation was applied to nonpregnant rats via a silastic disc implanted in the uterus. The disc abutted against the cervix and was attached to a thread externalized through the vaginal orifice. Application of a force of 150 g, but not 100 g, produced a significant increase in tail flick latency (110.4 +/- 40.6%, P less than 0.03). This effect was abolished by pelvic neurectomy, but was not altered by hypogastric neurectomy. Stimulation of the uterine cervix in combined pelvic and hypogastric neurectomy rats produced a decrease in tail flick latency. These results indicate that the analgesia that occurs during pregnancy and/or parturition may result, at least in part, from the uterocervical mechanostimulation that occurs during this condition.Brain Research 01/1992; 566(1-2):299-302. · 2.88 Impact Factor