Localization of nitric oxide synthase and haemoxygenase, and functional effects of nitric oxide and carbon monoxide in the pig and human intravesical ureter

Iselin, Christophe; Alm, Per; Schaad, Nicolas; Larsson, Bengt; Graber, Pierre; Andersson, Karl‐Erik

doi:10.1002/(sici)1520-6777(1997)16:3<209::aid-nau10>3.0.co;2-g

Cited by 25 publications

(10 citation statements)

References 36 publications

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“…By using shorter widths, similar to the currently used set‐up, TTX‐sensitive responses of the rat ureter are also described . Supporting our findings of partially TTX‐sensitive contractions, other authors that used similar stimulation parameters as we did in this study have also reported of TTX‐sensitive responses in human isolated ureters . Taken together with our findings that the TRP‐active compounds did not have effects on resting tension or contractions by K + , we suggest that capsaicin and the TRPA1‐agonists exert some of their effects on nerve‐generated signals that are involved in contractile functions of the isolated human ureter.…”

Section: Discussionsupporting

confidence: 88%

Transient receptor potential a1 (TRPA1) agonists inhibit contractions of the isolated human ureter

Weinhold

Hennenberg

Strittmatter

et al. 2017

Neurourology and Urodynamics

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Section: Discussionsupporting

confidence: 88%

Transient receptor potential a1 (TRPA1) agonists inhibit contractions of the isolated human ureter

Weinhold

Hennenberg

Strittmatter

et al. 2017

Neurourology and Urodynamics

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“…Laboratory Investigation • October 2000 • Volume 80 • Number 10 lack of effect of CO on human intravesical ureter (Iselin et al, 1997), and because the status of CO as a neurotransmitter remains uncertain, lack of HO enzymes in the human bladder might be expected.…”

Section: Detrusor Denervation In Spinal Cord Injurymentioning

confidence: 99%

Structural and Functional Denervation of Human Detrusor after Spinal Cord Injury

Drake

Hedlund

Mills

et al. 2000

Laboratory Investigation

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SUMMARY:The bladder receives an extensive nerve supply that is predominantly cholinergic, but several putative transmitters are present, some of which are colocalized. Previous studies have shown increased levels of sensory nerves, reduced inhibitory transmitters, and structural and functional changes in the excitatory input in unstable bladder conditions. The present study compared the end-organ nerve supply to the bladder in spinal cord injury (SCI) with uninjured controls. Acetylcholinesterase histochemistry and double-label immunofluorescence were used to investigate neurotransmitter content, with confocal laser scanning microscopy to assess colocalization. Organ bath studies provided functional correlates for the structural changes in the excitatory innervation. Control samples had dense innervation of the detrusor containing a diverse range of transmitters. Hyperreflexic SCI samples showed patchy denervation, and areflexic SCI samples were diffusely denervated. Vasoactive intestinal polypeptide-, neuropeptide Y-, neuronal nitric oxide synthase-, and galanin-immunoreactive nerve fibers were reduced from frequent or moderately frequent to infrequent or very infrequent in SCI. Calcitonin gene-related peptide-immunoreactive fibers were infrequent in controls and SCI samples. Patterns of colocalization were unchanged, but significantly fewer fibers expressed more than one transmitter. The subepithelial plexus was markedly reduced and several of the smaller coarse nerve trunks showed no immunoreactivity to the transmitters assessed. There was no reduction in sensitivity to electrical field stimulation of intrinsic nerves in SCI, but the maximum force generated by each milligram of bladder tissue and the peak force as a proportion of the maximum carbachol contraction were significantly reduced and the responses were protracted. There was no significant functional atropine-resistant neuromuscular transmission in controls or SCI. The reported findings have clinical implications in the management of chronic SCI and development of new treatments.

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“…NOS‐IR neurons in extramural ganglia and NOS‐containing nerve fibres travel within large extramural nerve trunks and march among smooth muscle bundles, in the subepithelium and around blood vessels. NOS is usually found in parasympathetic nerve fibres co‐localized with VIP and, to a minor extent, in sympathetic nerve fibres co‐localized with NPY, thus suggesting the involvement of a local inhibitory NO/VIP pathway in the co‐ordination of ureteral peristalsis and ureterovesical junction motility, for urine bolus discharge into urinary bladder .…”

Section: Nitric Oxide (No)mentioning

confidence: 99%

“…Regulation of the bladder and urethral outlet is dependent on three sets of peripheral nerves: parasympathetic, sympathetic and somatic nerves that contain afferent and efferent pathways . Strong evidence shows that the gaseous mediator NO, and also probably H 2 S would be involved in the NANC inhibitory transmission to the distal ureter, ureterovesical junction and bladder out‐flow region . This MiniReview was focused to the role played by NO and H 2 S in regulation of upper and lower urinary tract activity.…”

mentioning

confidence: 99%

The Role of Nitric Oxide and Hydrogen Sulfide in Urinary Tract Function

Fernandes

Hernández

2016

Basic Clin Pharma Tox

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This MiniReview focuses on the role played by nitric oxide (NO) and hydrogen sulfide (H 2 S) in physiology of the upper and lower urinary tract. NO and H 2 S, together with carbon monoxide, belong to the group of gaseous autocrine/paracrine messengers or gasotransmitters, which are employed for intra-and intercellular communication in almost all organ systems. Because they are lipid-soluble gases, gaseous transmitters are not constrained by cellular membranes, so that their storage in vesicles for later release is not possible. Gasotransmitter signals are terminated by falling concentrations upon reduction in production that are caused by reacting with cellular components (essentially reactive oxygen species and NO), binding to cellular components or diffusing away. NO and, more recently, H 2 S have been identified as key mediators in neurotransmission of the urinary tract, involved in the regulation of ureteral smooth muscle activity and urinary flow ureteral resistance, as well as by playing a crucial role in the smooth muscle relaxation of bladder outlet region. Urinary bladder function is also dependent on integration of inhibitory mediators, such as NO, released from the urothelium. In the bladder base and distal ureter, the co-localization of neuronal NO synthase with substance P and calcitonin gene-related peptide in sensory nerves as well as the existence of a high nicotinamide adenine dinucleotide phosphate-diaphorase activity in dorsal root ganglion neurons also suggests the involvement of NO as a sensory neurotransmitter.Ureteral peristalsis is initiated by spontaneous activity of renal pacemaker cells, also known as interstitial cells of Cajal-like cells, located in renal pelvis and proximal ureter, which generate pyeloureteric autorhythmicity of adjacent smooth muscle cells, thus favouring the conduction and amplification of ureteral smooth muscle electrical activity regulating ureteral peristalsis and smooth muscle tone [1]. Although ureteral peristalsis is essentially regulated by myogenic mechanisms, neurogenic factors also play an important role in this process. In fact, at distal ureter and ureterovesical junction, smooth muscle activity is regulated by the autonomic nervous system, via noradrenergic, cholinergic and non-adrenergic non-cholinergic (NANC) nerves [2,3].Filling and periodic expulsion of urine from bladder is regulated by a neural system in the brain and spinal cord that coordinates the reciprocal activity of two functional units in the lower urinary tract including a reservoir, the urinary bladder and an outlet region comprising bladder neck, urethra and striated muscles of the urethral sphincter. Regulation of the bladder and urethral outlet is dependent on three sets of peripheral nerves: parasympathetic, sympathetic and somatic nerves that contain afferent and efferent pathways [4]. Strong evidence shows that the gaseous mediator NO, and also probably H 2 S would be involved in the NANC inhibitory transmission to the distal ureter, ureterovesical junction and bladder ...

show abstract

Localization of nitric oxide synthase and haemoxygenase, and functional effects of nitric oxide and carbon monoxide in the pig and human intravesical ureter

Cited by 25 publications

References 36 publications

Transient receptor potential a1 (TRPA1) agonists inhibit contractions of the isolated human ureter

Transient receptor potential a1 (TRPA1) agonists inhibit contractions of the isolated human ureter

Structural and Functional Denervation of Human Detrusor after Spinal Cord Injury

The Role of Nitric Oxide and Hydrogen Sulfide in Urinary Tract Function

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