We have confirmed that hydrogen sulfide (H 2 S) is a possible relaxation factor in the rat bladder, and H 2 S-induced bladder relaxation is impaired in 18-week-old (18W) spontaneously hypertensive rats (SHRs), which show bladder dysfunctions. We compared effects of NaHS and GYY4137 (H 2 S donors) on bladder contractility and micturition reflex, and H 2 S contents and expression of enzymes related to H 2 S biosynthesis (CBS, MPST and CAT) in the bladder between 12W and 18W male SHRs. Effects of NaHS (1×10-8 to 3×10-4 M) were evaluated on carbachol (10-5 M)induced pre-contracted bladder strips. Under urethane-anesthesia, effects of intravesically instilled GYY4137 (10-8 to 10-6 M) on the rat micturition reflex were examined. The H 2 S contents and expression of CBS, MPST and CAT were measured by methylene blue method and western botting. Compared to 12W SHRs, NaHS-induced maximal relaxation of bladder strips was significantly decreased, GYY4137-induced intercontraction intervals prolongation was attenuated, the bladder H 2 S content and expression level of CBS, MPST and CAT in the bladder dome was higher in 18W SHRs. These results indicate that H 2 S-induced bladder relaxation in SHRs is impaired time-dependently, suggesting that early intervention in SHRs with H 2 S donors may prevent the development of hypertension-mediated bladder dysfunctions.
We recently reported that intracerebroventricularly (icv) administered epibatidine (EP), a nicotinic receptor (nAChR) agonist, inhibited the rat micturition reflex. We examined brain mechanisms of the EP-induced inhibition focusing on α4β2 and α7 nAChRs and GABA receptors in urethane-anesthetized (0.8 g/kg, ip) male Wistar rats (300-400 g). A catheter was inserted into the bladder to perform cystometrograms (CMG, 12 ml/h saline infusion). Three hours after the surgery, mecamylamine (MEC, an nAChR antagonist, 100 or 300 nmol/rat), DHβE (an α4β2 nAChR antagonist, 100 or 300 nmol/rat), MLA (an α7 nAChR antagonist, 30 or 100 nmol/rat) or SR95531 (SR, a GABA A receptor antagonist, 0.1 nmol/rat) was icv pretreated 30 min before EP administration (1 nmol/rat, icv).Effects of PHA568487 (PHA, an α7 nAChR agonist, 0.3 or 1 nmol/rat, icv) on the micturition reflex were also evaluated. Icv administered EP prolonged intercontraction intervals (ICI), an index of micturition frequency. The EPinduced prolongation was attenuated by pretreatment with MEC, MLA and SR, but not with DHβE. Similar to EP, PHA also prolonged ICI. These results suggest that brain α7 nAChR stimulation inhibits the rat micturition reflex via brain GABA A receptors.
Aims of study: Hydrogen sulfide (H 2 S), an endogenous gasotransmitter, modulates oxidative stress and inflammation.Therefore, we investigated effects of H 2 S on the bladder dysfunction in the cyclophosphamide (CYP)-induced cystitis in rats. Methods: Male Wistar rats (290-320g) were treated with saline or NaHS (H 2 S donor)/saline (10 μmol/kg/day, ip) once daily for one week before experiments. CYP (150 mg/kg, ip) or saline had been injected two days before the experiments. Under urethane-anesthesia (0.8 g/kg, ip), a catheter was inserted into the bladder via the bladder dome, continuous cystometry was performed (saline, 4 mL/h). Results: CYP reduced the body weight and increased bladder weight and bladder body weight ratio (BBR). Cystometric studies showed that CYP reduced intercontraction intervals (ICI) and bladder compliance (Com) along with an increase in the number of non-voiding contractions (NVCs). NaHS pretreatment significantly improved the CYP-induced changes in ICI, Com and the number of NVCs. However, NaHS showed no significant effect on CYPinduced changes in body weight, bladder weight or BBR. Conclusions: These data suggest that NaHS may have protective effects on CYP-induced bladder dysfunction.
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