Involvement of Purinergic Neurotransmission in Ketamine Induced Bladder Dysfunction

Meng, En; Chang, Han-Yu; Chang, Sun‐Yran; Sun, Guang‐Huan; Yü, Dah‐Shyong; Cha, Tai‐Lung

doi:10.1016/j.juro.2011.04.102

Cited by 64 publications

(64 citation statements)

References 17 publications

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“…Mice treated with ketamine for 8 weeks showed similar side effects and enhanced P2X1 receptor expression and non-cholinergic nerve-mediated contractions were demonstrated [483]. It was suggested that dysregulation of purinergic neurotransmission may underlie detrusor overactivity in ketamineinduced bladder dysfunction.…”

Section: Detrusor Overactivitymentioning

confidence: 96%

Purinergic signalling in the urinary tract in health and disease

Burnstock

2013

Purinergic Signalling

139

142

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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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Section: Detrusor Overactivitymentioning

confidence: 96%

Purinergic signalling in the urinary tract in health and disease

Burnstock

2013

Purinergic Signalling

139

142

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“…37 Another ketamine-treated mouse model discovered transmitters changed in the urinary bladder, whereby noncholinergic contractions and P2X1 receptor expression was enhanced. 38 This indicated dysregulation of purinergic neurotransmission, possibly giving rise to detrusor overactivity and bladder dysfunction.…”

Section: Clinical Featuresmentioning

confidence: 99%

Genitourinary toxicity of ketamine

Wei

Yang²,

Yin³

et al. 2013

Hong Kong Med J

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341Ketamine is a relatively new recreational drug used by youngsters in recent decades. Its toxic effects on the genitourinary system were first reported in 2007, and now attract extensive attention from urologists, pharmacologists, and toxicologists all over the world. As many front-line health professionals and medical social workers are still unaware of this new clinical entity and an increasing number of the drug users seek help for urological symptoms, this mini-review aimed to summarise the clinical features and possible mechanisms of ketamine-induced genitourinary toxicity. By raising public awareness of these toxic effects, the authors hope that the contents of this review will be widely disseminated not only to medical professionals, but also to relevant government departments and the general public. Genitourinary toxicity of ketamine

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“…In a mouse ketamine-addiction model, enhanced noncholinergic contractions and P2x1 receptor expression in the bladder indicated that dysregulation of purinergic neurotransmission might underlie detrusor overactivity. 7 Recent studies in KIC patients have shown increases in bladder mast cell and 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 eosinophil cell infiltration, with greater serum IgE levels than in controls and in acute bacterial cystitis patients, 8,9 revealing that KIC is associated with hypersensitivity and/or allergic reactions. Cyclooxygenase (COX)-2 is inducible in response to inflammatory stimuli, cytokines, 10 or endotoxins, 11 resulting in exaggerated release of prostanoids.…”

mentioning

confidence: 99%