Effects of anaesthesia on the nitrergic pathway during the micturition reflex in rats

Masuda, Hitoshi; Ogawa, Toshihide; Kihara, Kazunori; Chancellor, Michael B.; Groat, William C. de; Yoshimura, Naoki

doi:10.1111/j.1464-410x.2007.06872.x

Cited by 21 publications

(35 citation statements)

References 28 publications

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“…NO donors can also affect bladder afferent neuron excitability by modulating Ca 2ϩ channels (Yoshimura et al, 2001) and when administered intravesically NO donors can suppress bladder hyperactivity induced by cystitis (Ozawa et al, 1999). To test the involvement of NO in the observed OxoM effects, the NOS inhibitor L-NAME (Masuda et al, 2007) was administered before OxoM. L-NAME alone at 5 mg/kg and 25 mg/kg (i.v.)…”

Section: The Inhibitory Effects Of Intravesical Oxom Involve Nomentioning

confidence: 99%

“…7A). These effects lasted for Ͼ3-4 h and might be related to a block of NO mediated urethral smooth muscle relaxation and an increase in the urethral outlet resistance during micturition (Bennett et al, 1995;Masuda et al, 2007). Because 5 mg/kg L-NAME had fewer effects on CMG parameters (i.e., only the amplitude increased significantly from control; paired t test p Ͻ 0.05; n ϭ 9 rats), this dose was chosen for further studies.…”

Section: The Inhibitory Effects Of Intravesical Oxom Involve Nomentioning

confidence: 99%

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Activation of Muscarinic Receptors in Rat Bladder Sensory Pathways Alters Reflex Bladder Activity

Kullmann¹,

Artim²,

Birder³

et al. 2008

J. Neurosci.

103

110

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Antimuscarinic drugs affect bladder sensory symptoms such as urgency and frequency, presumably by acting on muscarinic acetylcholine receptors (mAChRs) located in bladder sensory pathways including primary afferent nerves and urothelium. However, the expression and the function of these receptors are not well understood. This study investigated the role of mAChRs in bladder sensory pathways in vivo in urethane anesthetized rats. Intravesical administration of the mAChR agonist oxotremorine methiodide (OxoM) elicited concentration-dependent excitatory and inhibitory effects on the frequency of voiding. These effects were blocked by intravesical administration of the mAChR antagonist atropine methyl nitrate (5 M) and were absent in rats pretreated with capsaicin to desensitize C-fiber afferent nerves. Low concentrations of OxoM (5 M) decreased voiding frequency by ϳ30%, an effect blunted by inhibiting nitric oxide (NO) synthesis with L-NAME (N -nitro-L-arginine methyl ester hydrochloride; 5 mg/kg; i.v.). High concentrations of OxoM (40 M) increased voiding frequency by ϳ45%, an effect blunted by blocking purinergic receptors with PPADS (0.1-1 mM; intravesically). mAChR agonists stimulated release of ATP from cultured urothelial cells. Intravenous administration of OxoM (0.01-5 g/kg) did not mimic the intravesical effects on voiding frequency. These results suggest that activation of mAChRs located near the luminal surface of the bladder affects voiding functions via mechanisms involving ATP and NO release presumably from the urothelium, that in turn could act on bladder C-fiber afferent nerves to alter their firing properties. These findings suggest that the urothelial-afferent nerve interactions can influence reflex voiding function.

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Section: The Inhibitory Effects Of Intravesical Oxom Involve Nomentioning

confidence: 99%

Section: The Inhibitory Effects Of Intravesical Oxom Involve Nomentioning

confidence: 99%

Activation of Muscarinic Receptors in Rat Bladder Sensory Pathways Alters Reflex Bladder Activity

Kullmann¹,

Artim²,

Birder³

et al. 2008

J. Neurosci.

103

110

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“…Creatinine corrected NGF levels in urine were correlated with bladder volume at urge sensation in the controls but pathologic elevation of NGF levels in OAB patients at lower bladder capacity precluded the significant association of NGF expression with urgency sensation at full bladder capacity (Liu and Kuo, 2009). Bladder stretching in rodents is expected to be higher with the increased bladder capacity under anesthesia (Masuda et al, 2007). Therefore, cyclic stretching and contraction of bladder during CMG was expected to increase the expression of NGF and its receptor.…”

Section: Discussionmentioning

confidence: 99%

Constitutive expression Of NGF And P75NTR affected by bladder distension and NGF antisense treatment

et al. 2016

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Aims It is known that bladder exposure to noxious stimuli elicits nerve growth factor (NGF) expression with region wise differences. Here, we investigated the effect of bladder distension (cystometry) and bladder wall injection of NGF antisense oligonucleotide (ODN) together as well as separately on spontaneous (constitutive) expression of NGF and its cognate p75 neurotrophin receptor (p75NTR). Method Under isoflurane anesthesia, either 15µg of protamine sulfate (vehicle) alone or complexed with 1.5µg of NGF antisense or scrambled ODN was injected (10µL) at 4 sites in bladder wall of 24 adult female Sprague-Dawley rats and 6 rats were left untreated (n=30). Under urethane anesthesia, cystometry (CMG) was performed in treated and control rats. Fluorescent ODN and NGF/p75NTR expression was localized in harvested tissue. Key findings Complexation of ODN with protamine was essential for the retention of ODN in bladder tissue as the uncomplexed ODN was untraceable after injection. Bladder distension from CMG raised the expression of NGF and p75NTR relative to CMG naïve rats. The groups treated with vehicle, scrambled and antisense ODN were indistinct with regard to CMG parameters, but the intense immunoreactivity of NGF and p75NTR seen in the vehicle and scrambled ODN groups was reduced following treatment with NGF antisense. Significance The constitutive expression of NGF and p75NTR is responsive to bladder distension and administration of NGF antisense. Complexation with protamine reduces the clearance of ODN and demonstrates the potential of ODN nanoparticles as an option for reducing the inducible NGF expression in OAB patients following intradetrusor injection.

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“…An NO scavenger, oxyhemoglobin, enhances bladder activity in the urothelium or suburothelially in normal conscious rats, suggesting that NO plays an important role in the regulation of afferent firing in the bladder . An overactive bladder is involved in excitability of bladder afferent C‐fibers . Several investigators have shown that the eNOS–NO–cGMP pathway could regulate the micturition reflex through the decrease in the excitability of bladder afferents .…”

Section: Luts/bph and Vascular Functionmentioning

confidence: 99%

Lower urinary tract symptoms/benign prostatic hypertrophy and vascular function: Role of the nitric oxide–phosphodiesterase type 5–cyclic guanosine 3′,5′‐monophosphate pathway

Higashi

2017

Int J of Urology

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It is well known that there is an association of lower urinary tract symptoms/ benign prostatic hypertrophy with cardiovascular disease, suggesting that lower urinary tract symptoms/benign prostatic hypertrophy is a risk factor for cardiovascular events. Vascular function, including endothelial function and vascular smooth muscle function, is involved in the pathogenesis, maintenance and development of atherosclerosis, leading to cardiovascular events. Vascular dysfunction per se should also contribute to lower urinary tract symptoms/benign prostatic hypertrophy. Both lower urinary tract symptoms/benign prostatic hypertrophy and vascular dysfunction have cardiovascular risk factors, such as hypertension, dyslipidemia, diabetes mellitus, aging, obesity and smoking. Inactivation of the phosphodiesterase type 5-cyclic guanosine 3 0 ,5 0 -monophosphate-nitric oxide pathway causes lower urinary tract symptoms/benign prostatic hypertrophy through an enhancement of sympathetic nervous activity, endothelial dysfunction, increase in Rho-associated kinase activity and vasoconstriction, and decrease in blood flow of pelvic viscera. Both endogenous nitric oxide and exogenous nitric oxide act as vasodilators on vascular smooth muscle cells through an increase in the content of cyclic guanosine 3 0 ,5 0 -monophosphate, which is inactivated by phosphodiesterase type 5. In a clinical setting, phosphodiesterase type 5 inhibitors are widely used in patients with lower urinary tract symptoms/benign prostatic hypertrophy. Phosphodiesterase type 5 inhibitors might have beneficial effects on vascular function through not only inhibition of cyclic guanosine 3 0 ,5 0 -monophosphate degradation, but also increases in testosterone levels and nitric oxide bioavailability, increase in the number and improvement of the function of endothelial progenitor cells, and decrease in insulin resistance. In the present review, the relationships between lower urinary tract symptoms/benign prostatic hypertrophy, the phosphodiesterase type 5-nitric oxidecyclic guanosine 3 0 ,5 0 -monophosphate pathway, vascular function and cardiovascular outcomes are examined.Key words: benign prostatic hypertrophy, lower urinary tract symptoms, nitric oxide, phosphodiesterase type 5-cyclic guanosine 3 0 ,5 0 -monophosphate, vascular function.

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Effects of anaesthesia on the nitrergic pathway during the micturition reflex in rats

Cited by 21 publications

References 28 publications

Activation of Muscarinic Receptors in Rat Bladder Sensory Pathways Alters Reflex Bladder Activity

Activation of Muscarinic Receptors in Rat Bladder Sensory Pathways Alters Reflex Bladder Activity

Constitutive expression Of NGF And P75NTR affected by bladder distension and NGF antisense treatment

Lower urinary tract symptoms/benign prostatic hypertrophy and vascular function: Role of the nitric oxide–phosphodiesterase type 5–cyclic guanosine 3′,5′‐monophosphate pathway

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