Effects of dimethyl sulphoxide and heparin on stretch‐activated ATP release by bladder urothelial cells from patients with interstitial cystitis

Sun, Yue; Chai, Toby C.

doi:10.1046/j.1464-410x.2002.02912.x

Cited by 48 publications

(32 citation statements)

References 29 publications

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“…One is that purinergic nerve-mediated contraction of the human bladder is increased to 40% in pathophysiological conditions such as interstitial cystitis, outflow obstruction, idiopathic detrusor instability, and probably also neurogenic bladder (Wammack et al, 1995;Andersson, 1997;Andersson and Hedlund, 2002). ATP release from bladder epithelial cells from patients with interstitial cystitis is significantly greater than that from healthy cells (Sun and Chai, 2002), and there is a change in expression of both P2X and P2Y receptors in urothelial cells (Birder et al, 2004;Tempest et al, 2004). P2X 1 receptor subtype expression markedly increased in obstructed bladder (Boselli et al, 2001) and in the absence of P2X 3 receptors in mouse knockouts, the bladder is hyperactive (Cockayne et al, 2000;Vlaskovska et al, 2001).…”

Section: B Lower Urinary Tractmentioning

confidence: 99%

Pathophysiology and Therapeutic Potential of Purinergic Signaling

2006

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Section: B Lower Urinary Tractmentioning

confidence: 99%

Pathophysiology and Therapeutic Potential of Purinergic Signaling

2006

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“…Both resting and evoked ATP release from urothelial cells was significantly higher after chronic spinal cord injury [644]. In paraplegic patients with suprasacral lesions, the management of urinary incontinence resulting from hyperreflexic detrusor contraction is a frequent problem.…”

Section: Detrusor Overactivitymentioning

confidence: 99%

“…It was suggested that enhanced penetration of endogenous ATP due to urothelial damage may contribute to urinary frequency and bladder pain in hypersensitive bladder in BPS/ IC [524]. Urothelial cells from patients with IC released significantly more ATP in response to stretch than did control cells [644]. Further, the authors showed that the stretchactivated ATP release was blocked by adding dimethyl sulphoxide or heparin, both intravesical agents commonly used to treat the symptoms of IC.…”

Section: Detrusor Overactivitymentioning

confidence: 99%

Purinergic signalling in the urinary tract in health and disease

Burnstock

2013

Purinergic Signalling

140

149

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Purinergic signalling is involved in a number of physiological and pathophysiological activities in the lower urinary tract. In the bladder of laboratory animals there is parasympathetic excitatory cotransmission with the purinergic and cholinergic components being approximately equal, acting via P2X1 and muscarinic receptors, respectively. Purinergic mechanosensory transduction occurs where ATP, released from urothelial cells during distension of bladder and ureter, acts on P2X3 and P2X2/3 receptors on suburothelial sensory nerves to initiate the voiding reflex, via low threshold fibres, and nociception, via high threshold fibres. In human bladder t h e p u r i n e rg i c c o m p o n e n t o f p a r a s y m p a t h e t i c cotransmission is less than 3 %, but in pathological conditions, such as interstitial cystitis, obstructed and neuropathic bladder, the purinergic component is increased to 40 %. Other pathological conditions of the bladder have been shown to involve purinoceptor-mediated activities, including multiple sclerosis, ischaemia, diabetes, cancer and bacterial infections. In the ureter, P2X7 receptors have been implicated in inflammation and fibrosis. Purinergic therapeutic strategies are being explored that hopefully will be developed and bring benefit and relief to many patients with urinary tract disorders.

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“…P2X 3 -and P2X 3 /P2X 2 -deficient mice have problems with the micturition response, proving these findings with mouse genetics [64,65,79,83]. Chai and Sun have shown that ATP release and signaling process is heightened in interstitial cystitis (IC) [63,77]. There are also alterations in P2 receptor expression in IC [70,74].…”

Section: Tls Of Henlementioning

confidence: 99%

Purinergic signaling in the lumen of a normal nephron and in remodeled PKD encapsulated cysts

Hovater

Olteanu

Welty

et al. 2008

Purinergic Signalling

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The nephron is the functional unit of the kidney. Blood and plasma are continually filtered within the glomeruli that begin each nephron. Adenosine 5′ triphosphate (ATP) and its metabolites are freely filtered by each glomerulus and enter the lumen of each nephron beginning at the proximal convoluted tubule (PCT). Flow rate, osmolality, and other mechanical or chemical stimuli for ATP secretion are present in each nephron segment. These ATP-release stimuli are also different in each nephron segment due to water or salt permeability or impermeability along different luminal membranes of the cells that line each nephron segment. Each of the above stimuli can trigger additional ATP release into the lumen of a nephron segment. Each nephron-lining epithelial cell is a potential source of secreted ATP. Together with filtered ATP and its metabolites derived from the glomerulus, secreted ATP and adenosine derived from cells along the nephron are likely the principal two of several nucleotide and nucleoside candidates for renal autocrine and paracrine ligands within the tubular fluid of the nephron. This minireview discusses the first principles of purinergic signaling as they relate to the nephron and the urinary bladder. The review discusses how the lumen of a renal tubule presents an ideal purinergic signaling microenvironment. The review also illustrates how remodeled and encapsulated cysts in autosomal dominant polycystic kidney disease (ADPKD) and remodeled pseudocysts in autosomal recessive PKD (ARPKD) of the renal collecting duct likely create an even more ideal microenvironment for purinergic signaling. Once trapped in these closed microenvironments, purinergic signaling becomes chronic and likely plays a significant epigenetic and detrimental role in the secondary progression of PKD, once the remodeling of the renal tissue has begun. In PKD cystic microenvironments, we argue that normal purinergic signaling within the lumen of the nephron provides detrimental acceleration of ADPKD once remodeling is complete.

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Effects of dimethyl sulphoxide and heparin on stretch‐activated ATP release by bladder urothelial cells from patients with interstitial cystitis

Cited by 48 publications

References 29 publications

Pathophysiology and Therapeutic Potential of Purinergic Signaling

Pathophysiology and Therapeutic Potential of Purinergic Signaling

Purinergic signalling in the urinary tract in health and disease

Purinergic signaling in the lumen of a normal nephron and in remodeled PKD encapsulated cysts

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