Feline interstitial cystitis results in mechanical hypersensitivity and altered ATP release from bladder urothelium

Birder, Lori A.; Barrick, Stacey; Roppolo, James R.; Kanai, Anthony; Groat, William C. de; Kiss, Susanna; Buffington, C.A. Tony

doi:10.1152/ajprenal.00056.2003

Cited by 197 publications

(226 citation statements)

References 30 publications

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“…In the present study, 3 H-ACh evoked release was unmasked by atropine suggesting this was mediated by activation of nicotinic receptors. In addition, similar to that reported in other types of non-neuronal cells ), stimulation of acetylcholine-receptors in bladder urothelial cells results in a release of nitric oxide, prostanoids (unpublished observations) and ATP (Birder et al, 2003).…”

Section: Discussionsupporting

confidence: 85%

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Non-neuronal acetylcholine and urinary bladder urothelium

et al. 2007

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Non-neuronal release of acetylcholine (ACh) has been proposed to play a role in urinary bladder function. These studies investigated the expression and function of the non-neuronal cholinergic system in cultured urothelial cells isolated from the rat urinary bladder. Our findings have revealed that urothelial cells express the high-affinity choline transporter (CHT1) and acetylcholine synthesizing enzymes, choline acetyltransferase (ChAT) and carnitine acetyltransferase (CarAT). In contrast to neurons, urothelial cells do not express the vesicular acetylcholine transporter (VAChT) but do express OCT3, a subtype of polyspecific organic cation transporter (OCT) that is thought to be involved in the release of acetylcholine from nonneuronal cells. Following exposure of cultured urothelial cells to 3 H-choline, radioactivity was detected in the cells and increased release of radioactivity into the eternal media was evoked by mechanical stimulation (exposure of the cells to 50% hypotonic Krebs) or chemical stimulation of purinergic receptors by 100 μM ATP. The present experiments did not establish if the evoked release of radioactivity (termed 3 HACh release in this paper) was due to release of acetylcholine or choline. 3 H-ACh release was not evoked by application of acetylcholine alone, however pretreatment with the non-selective muscarinic receptor antagonist atropine prior to application of acetylcholine facilitated 3 H-ACh release, suggesting that the acetylcholine released from urothelial cells may participate in a negative feedback mechanism by acting on muscarinic receptors to inhibit its own release in the urothelium. Brefeldin, an agent which disrupts vesicular exocytosis, did not block hypotonicevoked 3 H-ACh release. These observations indicate that acetylcholine release from urothelial cells is mediated by different mechanisms than those such as vesicular storage and exocytosis that underlie the release of neurotransmitters from nerves.

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Section: Discussionsupporting

confidence: 85%

“…Preparation of urothelial cultures was carried out as previously described (Birder et al, 2003;Birder et al, 2002). Briefly, bladders were excised from adult female Sprague-Dawley rats (250-350 g), killed by inhalation of medical grade CO 2 followed by thoracotomy and cardiac puncture.…”

Section: Cell Culturementioning

confidence: 99%

Non-neuronal acetylcholine and urinary bladder urothelium

et al. 2007

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“…receptors and ion channels) that have been identified in the urothelium include receptors for bradykinin, neurotrophins (Trk-A and p75), purines (P2X and P2Y), norepinephrine (α and β), acetylcholine (nicotinic and muscarinic receptors), protease-activated receptors, amiloride-sensitive and mechanosensitive Na + channels, and a number of transient receptor potential (TRP) channels (TRPV1, TRPV2, TRPV4, TRPM8) ( Table 1). [28][29][30][31][32][33][34][35][36][37][38] …”

Section: Signaling Role Of the Urotheliummentioning

confidence: 99%

“…33 P2X and P2Y purinergic receptor subtypes are expressed in cells (urothelium, nerves and myofibroblasts) that are located at or near the luminal surface of the bladder, which suggests that ATP has an important role in chemical communication in the bladder. Basolateral ATP release from urothelial cells following either chemical or mechanical stimuli 21,29,32 might signal to adjacent urothelial cells as well as to other cell types (myofibroblasts or bladder nerves) within the submucosa (Figure 1). In addition, the close proximity of urothelial cells to myofibroblasts and bladder nerves, the sensitivity of these cells to ATP (indicated by an ATP-induced increase in intracellular Ca 2+ in afferent neurons, urothelial cells and myofibroblasts), and the evidence for cell-cell coupling mediated by gap junctions provide support for a number of physical and chemical interactions that could influence bladder function.…”

Section: Role Of Different Receptors and Substances In Urothelial Funmentioning

confidence: 99%

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Mechanisms of Disease: involvement of the urothelium in bladder dysfunction

2007

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SUMMARYAlthough the urinary bladder urothelium has classically been thought of as a passive barrier to ions and solutes, a number of novel properties have been recently attributed to urothelial cells. Studies have revealed that the urothelium is involved in sensory mechanisms (i.e. the ability to express a number of sensor molecules or respond to thermal, mechanical and chemical stimuli) and can release chemical mediators. Localization of afferent nerves next to the urothelium suggests that urothelial cells could be targets for neurotransmitters released from bladder nerves or that chemicals released by urothelial cells could alter afferent nerve excitability. Taken together, these and other findings highlighted in this article suggest a sensory function for the urothelium. Elucidation of mechanisms that influence urothelial function might provide insights into the pathology of bladder dysfunction.

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Neural Control of the Lower Urinary Tract

Groat

Griffiths

Yoshimura

2014

Comprehensive Physiology

350

527

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This article summarizes anatomical, neurophysiological, pharmacological, and brain imaging studies in humans and animals that have provided insights into the neural circuitry and neurotransmitter mechanisms controlling the lower urinary tract. The functions of the lower urinary tract to store and periodically eliminate urine are regulated by a complex neural control system in the brain, spinal cord, and peripheral autonomic ganglia that coordinates the activity of smooth and striated muscles of the bladder and urethral outlet. The neural control of micturition is organized as a hierarchical system in which spinal storage mechanisms are in turn regulated by circuitry in the rostral brain stem that initiates reflex voiding. Input from the forebrain triggers voluntary voiding by modulating the brain stem circuitry. Many neural circuits controlling the lower urinary tract exhibit switch-like patterns of activity that turn on and off in an all-or-none manner. The major component of the micturition switching circuit is a spinobulbospinal parasympathetic reflex pathway that has essential connections in the periaqueductal gray and pontine micturition center. A computer model of this circuit that mimics the switching functions of the bladder and urethra at the onset of micturition is described. Micturition occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary micturition, leading to urinary incontinence. Neuroplasticity underlying these developmental and pathological changes in voiding function is discussed.

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Feline interstitial cystitis results in mechanical hypersensitivity and altered ATP release from bladder urothelium

Cited by 197 publications

References 30 publications

Non-neuronal acetylcholine and urinary bladder urothelium

Non-neuronal acetylcholine and urinary bladder urothelium

Mechanisms of Disease: involvement of the urothelium in bladder dysfunction

Neural Control of the Lower Urinary Tract

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