Responses Of Rat Urinary Bladder Research Articles

Donepezil-induced response of Spirulina supplemented rat urinary bladder

At present, very little is known about the effects of donepezil on vascular reactivity. The aim of the present study was to evaluate the responses of rat urinary bladder to donepezil (10-10-3x10-4 M) and the role of Spirulina supplementation in these effects. Animals were divided into the two groups of six animals in each group. The first group received only distilled water daily as vehicle for six weeks and served as the control. The second group received Spirulina 750 mg kg -1 orally, daily for six weeks and served as the spirulina group. Preparations of rat urinary bladder were used from both groups. Donepezil produced concentration dependent relaxation of rat urinary bladder preparations pre-contracted with KCl.The pIC50 value, but not the maximal response of donepezil, was significantly lower (p<0.05) in the Spirulina supplemented group. These results demonstrated for the first time that spirulina treatment can affect urinary bladder activity (Fig. 1, Ref. 20).

Montelukast reduces ischaemia/reperfusion-induced bladder dysfunction and oxidant damage in the rat

The present study aimed to investigate the possible beneficial effects of the cysteinyl leukotriene-1 receptor antagonist montelukast on contractility and oxidant damage after ischaemia/reperfusion (I/R) of rat urinary bladder. The abdominal aorta of Sprague-Dawley rats was occluded to induce I/R. Montelukast (10 mg kg(-1)) or saline was administered intraperitoneally before I/R. In the sham-operated group, the abdominal aorta was left intact and the animals were treated with montelukast or saline. After decapitation, the bladder was removed and the tissue was either used for functional studies or stored for biochemical assays. In the I/R group, the isometric contractile responses of the bladder strips to carbachol (10(-8)-10(-4) M) were lower than those of the control group and were reversed by treatment with montelukast. Lipid peroxidation and myeloperoxidase activity of the bladder tissues in the I/R group were greater than in the sham-operated group. Montelukast treatment in the I/R group decreased these parameters compared with I/R alone. Similarly, the significant decrease in tissue glutathione level in the I/R group compared with controls was also prevented by montelukast. Treatment with montelukast almost completely reversed the low contractile responses of rat urinary bladder to carbachol and prevented oxidative tissue damage following I/R.

IN VITRO FUNCTIONAL PROPERTIES OF THE RAT BLADDER REGENERATED BY THE BLADDER ACELLULAR MATRIX GRAFT

Purpose To assess the response of rat urinary bladder regenerated by the homologous bladder acellular matrix graft (BAMG) to in vitro electrical and pharmacologic stimuli. Materials and Methods In Sprague-Dawley rats, partial cystectomy (>50%) was performed, followed by BAMG augmentation cystoplasty. After 4 months, organ bath studies of tissue strips in 10 were used to compare the contractility of the BAMG regenerates and the corresponding host detrusor smooth muscle. Results The BAMG regenerates exhibited contractile activity to electrical field stimulation and a qualitatively identical pattern of response to muscarinic, purinergic, alpha- and beta-adrenergic drug administration and nitric oxide. At 4 months after surgery, the maximum forces of contraction of the BAMG regenerates to carbachol stimulation amounted to close to 80% of the host bladder response. With electrical field stimulation, they equaled 44% and 62% of the host bladder response after 2.5 and 4 months, respectively. Histological and immunohistochemical studies confirmed the presence of receptors for neurotransmitters that these functional in vitro studies implied. Conclusions The present study provides further evidence that augmentation cystoplasty with the BAMG leads to functional regeneration of the rat bladder detrusor smooth muscle.

Effect of substance P and capsaicin on urinary bladder of diabetic rats and the role of the epithelium

The in vitro responses of rat urinary bladder, to substance P and capsaicin were studied at 1, 4, 16, and 26 weeks of diapetes induction by streptozotocin. We also studied the role of epithelium in these responses. The results were compared with those obtained in age-matched control rats. The bladder contractile response to exogenous substance P was similar in both groups at all stages (1–26 weeks) studied, whereas the bladder response to capsaicin gradually decreased with the progression of diabetes. Atropine did not inhibit these responses whereas indomethacin slightly reduced substance P- but not capsaicin-induced responses in control and diabetic rats. The removal of epithelium slightly increased the substance P- and capsaicin-induced responses in control tissue; these responses were significantly reduced in tissue excised from diabetic rats. Our results indicate that, in rat urinary bladder, diabetes (1) provokes an impairment of capsaicin-sensitive sensory fibers but not of the cholinergic system even at an early stage (4 weeks) of the disease, (2) has no effect on the sensitivity of smooth muscle cells to substance P, (3) stimulates the release of epithelial contracting factors, partially non-prostanoic. Furthermore epithelium removal impairs acetylcholine-induced contraction in bladder excised from diabetic rats but not in controls.

The effects of Bay K 8644 and nifedipine on the responses of rat urinary bladder to electrical field stimulation, β,γ‐methylene ATP and acetylcholine

1. Bay K 8644 (0.33 nM to 1 microM) greatly increased the contractions of rat urinary bladder detrusor muscle induced by beta, gamma-methylene ATP (beta, gamma-MeATP, 10 microM) and by electrical field stimulation of the purinergic component (the cholinergic response was blocked by atropine). 2. The contractions induced by acetylcholine (ACh, 10 microM) and by electrical field stimulation of the cholinergic component (the purinergic response was blocked following desensitization by alpha, beta-MeATP) were also potentiated by Bay K 8644, although to a lesser extent than the purinergic responses. 3. Nifedipine (1 nM to 3.3 microM) inhibited all the contractions induced by beta, gamma-MeATP, ACh and electrical field stimulation. However, while the responses to beta, gamma-MeATP and electrical field stimulation of the purinergic component were almost abolished, a substantial proportion of the responses to ACh and electrical field stimulation of the cholinergic component were nifedipine resistant. 4. The concentration-effect curves for the potentiation by Bay K 8644 of the responses to beta, gamma-MeATP, ACh and electrical field stimulation were shifted to the right by nifedipine (10 nM). At concentrations greater than 1 microM, Bay K 8644 inhibited contraction. 5. It is concluded that voltage-sensitive calcium channels play an important role in the excitatory mechanical action of P2X-purinoceptor-mediated purinergic responses in the rat urinary bladder, while cholinergic-mediated responses are less dependent on such channels.