ArticleNeurourology and urodynamics2011
Developmental and spinal cord injury-induced changes in nitric oxide-mediated inhibition in rat urinary bladder.
Article in Neurourology and urodynamics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Targeting neurotrophin and nitric oxide signaling to treat spinal cord injury and associated neurogenic bladder overactivity.Continence (Amsterdam, Netherlands) · 2022Article
- Involvement of TRPM4 in detrusor overactivity following spinal cord transection in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Role of proNGF/p75 signaling in bladder dysfunction after spinal cord injury.The Journal of clinical investigation · 2018Article
- Urothelial proliferation and regeneration after spinal cord injury.American journal of physiology. Renal physiology · 2017Article
- Tanshinone IIA improves functional recovery in spinal cord injury-induced lower urinary tract dysfunction.Neural regeneration research · 2017Article
- Effect of phosphodiesterase inhibitors in the bladder.Asian journal of urology · 2015Review
- Bladder smooth muscle strip contractility as a method to evaluate lower urinary tract pharmacology.Journal of visualized experiments : JoVE · 2014Article
- The impact of discrete modes of spinal cord injury on bladder muscle contractility.BMC urology · 2013Article
- Nitric oxide modulates bladder afferent nerve activity in the in vitro urinary bladder-pelvic nerve preparation from rats with cyclophosphamide induced cystitis.Brain research · 2013Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
aimsDuring postnatal development large amplitude spontaneous activity of the neonatal rat bladder changes to a low amplitude adult pattern of activity that leads to improved storage function. Previously, we have shown that spontaneous activity in neonatal rat bladder strips is inhibited by activation of the nitric oxide (NO)-cGMP signaling pathway. In the present experiments we determined if this inhibitory pathway is altered during postnatal development or spinal cord injury.
methodsBaseline tone and amplitude and frequency of spontaneous contractions were measured in bladder strips from male or female neonatal (days 10-21), juvenile (days 24-39) and adult female spinal cord intact or chronic spinal cord injured Sprague-Dawley rats.
resultsThe inhibitory effects of an NO donor (SNAP) and a PDE-5 inhibitor (zaprinast) on spontaneous activity of bladder strips decreased during postnatal development, while an inhibitory effect of 8-bromo-cGMP, which was blocked by a protein kinase G inhibitor, was detected at all ages tested. However, the effect of NO-cGMP signaling to reduce baseline tone emerged during postnatal development. The inhibition induced by the NO donor was blocked by an inhibitor of soluble guanylyl cyclase (sGC). Chronic spinal cord injury (cSCI), which causes the re-emergence of a neonatal-like pattern of spontaneous activity, did not restore sensitivity to NO-mediated inhibition in adult rat bladders.
conclusionsThese data indicate that while cGMP signaling inhibits activity in young and adult bladders as well as after cSCI, there is a developmental decrease in the sensitivity of bladder to NO-mediated inhibition.
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