Prostaglandin E<sub>2</sub> release from isolated bladder strips in rats with spinal cord injury

Masunaga, Koichi; Yoshida, Masaki; Inadome, Akito; Iwashita, Hitoshi; Miyamae, Koichi; Ueda, Shoichi

doi:10.1111/j.1442-2042.2006.01274.x

Cited by 43 publications

(44 citation statements)

References 27 publications

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“…This is consistent with the notion that aberrant PG production contributes to the pathological conditions in the urinary bladder. Moreover, PGE 2 release by the urothelium was also found to be significantly higher in spinal cord-injured rats that present with bladder overactivity (112). These observations further indicate an important role of the urothelium-derived PGs in maintaining the normal function of urinary bladder.…”

Section: Urinary Tractsupporting

confidence: 58%

“…As demonstrated in the urinary bladder and airways, the release of PGs by the epithelium is sensitive to mechanical stimulation (47,111,112,135). This is of particular interest since many epithelial cells are exposed to dynamically changing environment and thus constantly under mechanical stimulations, such as the air flow in the airways and the increased pressure after food filling in the stomach and GI tract.…”

Section: Figure 3 Regulation Of Smooth Muscle Contraction By the Epmentioning

confidence: 99%

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Regulation of Smooth Muscle Contraction by the Epithelium: Role of Prostaglandins

2011

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As an analog to the endothelium situated next to the vascular smooth muscle, the epithelium is emerging as an important regulator of smooth muscle contraction in many vital organs/tissues by interacting with other cell types and releasing epithelium-derived factors, among which prostaglandins have been demonstrated to play a versatile role in governing smooth muscle contraction essential to the physiological and pathophysiological processes in a wide range of organ systems. As widely distributed throughout the body, including the blood vessels, airways, gastrointestinal, urinary, and reproductive tracts, smooth muscles have a variety of critical functions such as controlling blood pressure, respiration, and gastrointestinal peristalsis. Abnormality in smooth muscle contractility results in various disorders and diseases including hypertension, asthma, and dyspepsia (89, 95,179). Therefore, smooth muscle contraction is tightly regulated. Apart from the long-recognized regulation by neurotransmitters released from the innervating nerve endings or hormones from the blood stream nearby (66), smooth muscle contraction has been known, for over three decades, to be regulated by the endothelium lining the blood vessels with nitric oxide (NO) as the most important endothelial-derived factor (51, 121). Over recent decades, evidence has also been accumulated indicating an important role of the epithelium, the cell layer lining the luminal surface of many organs or tracts, such as the trachea/bronchus, stomach, intestine, bladder, and reproductive organs, in the regulation of smooth muscle contraction, with a number of epithelium-derived factors identified. However, the importance of the epithelium in regulating smooth muscle tones has not been adequately appreciated. In this review, we will examine the evidence collected from a number of organ systems and hope to provide a clearer picture as to how the epithelium acts as an indispensable regulator of smooth muscle contraction, with epithelium-derived prostaglandins (PGs) as the key mediators, participating in many vital physiological processes as well as the pathogenesis of many diseases.

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Section: Urinary Tractsupporting

confidence: 58%

Section: Figure 3 Regulation Of Smooth Muscle Contraction By the Epmentioning

confidence: 99%

Regulation of Smooth Muscle Contraction by the Epithelium: Role of Prostaglandins

2011

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“…It is known that PGs are released from the urinary bladder into the general circulation in response to disThe cardiovascular and gastrointestinal adverse effects of cyclooxygenase inhibitors seems to be a major concern that restricts their use in the treatment of urinary bladder dysfunction tension. PGs originate from the urothelium and the muscle layer of the urinary bladder [3,4]. PG synthesis is initiated by several factors, as follow: 1) detrusor muscle stretching, 2) urinary bladder autonomic nerve fibers stimulation, 3) urinary bladder mucosal damage, and 4) inflammatory mediators (e.g.…”

mentioning

confidence: 99%

“…PGs originate from the urothelium and the muscle layer of the urinary bladder [3,4]. PG synthesis is initiated by several factors, as follow: 1) detrusor muscle stretching, 2) urinary bladder autonomic nerve fibers stimulation, 3) urinary bladder mucosal damage, and 4) inflammatory mediators (e.g.…”

mentioning

confidence: 99%

The cardiovascular and gastrointestinal adverse effects of cyclooxygenase inhibitors seems to be a major concern that restricts their use in the treatment of urinary bladder dysfunction

Juszczak¹,

Drewa²

2015

CEJU

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Editorial referring to the paper: Gokkaya CS, Aktas BK, Ozden C, Bulut S, Karabakan M, Erkmen AE, Memis A. Flurbiprofen alone and in combination with alfuzosin for the management of lower urinary tract symptoms. Cent European J Urol. 2015; 68: 51-56.Flurbiprofen is a non-selective cyclooxygenase (COX) inhibitor, which inhibits the activity of both isoforms of COX (1 and 2). Also, flurbiprofen is one of the most potent non-steroidal anti-inflammatory agent (NSAIDs) in terms of prostaglandin inhibitory activity via reversible inhibition of COX, the enzyme responsible for the conversion of arachidonic acid to prostaglandin G2 (PGG2) and PGG2 to prostaglandin H2 (PGH2). COX exists as two isoforms, constitutive COX-1 and inducible COX-2. Prostaglandins (PGs) formed by COX-1 are primarily involved in the regulation of homeostatic functions in physiological processes, whereas PGs formed by COX-2 primarily mediate pain, inflammation, and cancer pathophysiology (e.g. prostate cancer) [1]. Aktas et al. [2] investigated the effectiveness and safety of flurbiprofen alone or in combination with alfuzosin, in the treatment of lower urinary tract symptoms suggestive of benign prostate obstruction (LUTS/BPO). The results showed that flurbiprofen increases the therapeutic effectiveness of alfuzosin by further improving symptoms in patients with LUTS/BPO. Combination therapy also improves urine flow compared to baseline. However, no superiority of monotherapy with flurbiprofen to alfuzosin is observed. Additionally, gastrointestinal adverse events are predominant in patients using flurbiprofen. PGs contribute to urinary bladder physiology. It is known that PGs are released from the urinary bladder into the general circulation in response to disThe cardiovascular and gastrointestinal adverse effects of cyclooxygenase inhibitors seems to be a major concern that restricts their use in the treatment of urinary bladder dysfunction tension. PGs originate from the urothelium and the muscle layer of the urinary bladder [3,4]. PG synthesis is initiated by several factors, as follow: 1) detrusor muscle stretching, 2) urinary bladder autonomic nerve fibers stimulation, 3) urinary bladder mucosal damage, and 4) inflammatory mediators (e.g. due to neurogenic inflammation) [5]. Numerous studies describing the effects of PGs in the urinary bladder have been published. It was reported that exogenous PGs alter urinary bladder motor activity in in vitro and in vivo studies. A link between PGs and the muscarinic system has been described previously [6]. Nile et al. [7] observed, in animal models, that ATP can activate PGE2 production by a complex mechanism, involving the purinergic receptors P2X and P2Y. Moreover, the response was inhibited by indomethacin (a non-selective COX inhibitor) and decreased the cholinergically stimulated autonomous contractions in the isolated bladder. PGs seem to affect the normal activity of the parasympathetic branch of the autonomic nervous system of the urinary bladder. In patients with overactive bladder (OAB) a hi...

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“…Bladder distension is a natural mechanical stimulus to evoke sensations such as fullness, urgency, and pain while the literature suggests a complex regulatory role of prostaglandins (PGs) in multiple aspects of urinary bladder physiology/pathophysiology. PGE 2 , one of the principal PGs, is synthesized in urothelium and detrusor smooth muscle (19,24,25,27) as well as in neurons and glial cells (18,23) and is released in response to various physiological (e.g., bladder distension) and pathological (e.g., mediators of inflammation) stimulation. PGE 2 interacts with four EP receptor subtypes (EP 1 , EP 2 , EP 3 , and EP 4 ) (23).…”

mentioning

confidence: 99%

An excitatory role for peripheral EP₃ receptors in bladder afferent function

Su¹,

Lashinger²,

Leon³

et al. 2008

American Journal of Physiology-Renal Physiology

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The excitatory roles of EP3 receptors at the peripheral afferent nerve innervating the rat urinary bladder have been evaluated by using the selective EP3 antagonist (2E)-3-{1-[(2,4-dichlorophenyl)methyl]-5-fluoro-3-methyl-1H-indol-7-yl}-N-[(4,5-dichloro-2-thienyl)sulfonyl]-2-propenamide (DG-041). The bladder rhythmic contraction model and a bladder pain model measuring the visceromotor reflex (VMR) to urinary bladder distension (UBD) have been used to evaluate DG-041 in female rats. In addition, male rats [spontaneously hypertensive rat (SHR), WistarKyoto (WKY), and Sprague-Dawley (SD)] were anesthetized with pentobarbital sodium, and primary afferent fibers in the L 6 dorsal root were isolated for recording the inhibitory response to UBD following intravenous injection of DG-041. Intravenous injection of DG-041 (10 mg/kg), a peripherally restricted EP 3 receptor antagonist, significantly reduced the frequency of bladder rhythmic contraction and inhibited the VMR response to bladder distension. The magnitude of reduction of the VMR response was not different in the different strains of rats (SD, SHR, and WKY). Furthermore, quantitative characterization of the mechanosensitive properties of bladder afferent nerves in SHR, WKY, and SD rats did not show the SHR to be supersensitive to bladder distension. DG-041 selectively attenuated responses of mechanosensitive afferent nerves to UBD, with strong suppression on the slow-conducting, high-threshold afferent fibers, with equivalent activity in the three strains. We conclude that sensitization of afferent nerve activity was not one of the mechanisms of bladder hypersensitivity in SHR. EP 3 receptors are involved in the regulation of bladder micturition and bladder nociception at the peripheral level.EP3; viscermotor reflex; bladder rhythmic contraction; bladder distension; afferent nerve SENSATION ASSOCIATED WITH the urinary bladder is conveyed primarily by pelvic and hypogastric nerves, by which the signal is relayed to the central nervous system (CNS). Most afferent fibers innervating the musculature of the bladder body pass through the pelvic nerve, whereas the majority of afferent endings in the bladder submucosa are derived from the hypogastric nerve (41), suggesting that the afferent fibers in the pelvic and hypogastric nerves have different roles, signaling mechanical stimulation (e.g., bladder distension) and chemical stimulation (e.g., inflammation), respectively (20,22,30,34). Bladder distension is a natural mechanical stimulus to evoke sensations such as fullness, urgency, and pain while the literature suggests a complex regulatory role of prostaglandins (PGs) in multiple aspects of urinary bladder physiology/pathophysiology. PGE 2 , one of the principal PGs, is synthesized in urothelium and detrusor smooth muscle (19,24,25,27) as well as in neurons and glial cells (18,23) and is released in response to various physiological (e.g., bladder distension) and pathological (e.g., mediators of inflammation) stimulation. PGE 2 interacts with four EP receptor subt...

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Prostaglandin E₂ release from isolated bladder strips in rats with spinal cord injury

Cited by 43 publications

References 27 publications

Regulation of Smooth Muscle Contraction by the Epithelium: Role of Prostaglandins

Regulation of Smooth Muscle Contraction by the Epithelium: Role of Prostaglandins

The cardiovascular and gastrointestinal adverse effects of cyclooxygenase inhibitors seems to be a major concern that restricts their use in the treatment of urinary bladder dysfunction

An excitatory role for peripheral EP₃ receptors in bladder afferent function

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Prostaglandin E2 release from isolated bladder strips in rats with spinal cord injury

Cited by 43 publications

References 27 publications

Regulation of Smooth Muscle Contraction by the Epithelium: Role of Prostaglandins

Regulation of Smooth Muscle Contraction by the Epithelium: Role of Prostaglandins

The cardiovascular and gastrointestinal adverse effects of cyclooxygenase inhibitors seems to be a major concern that restricts their use in the treatment of urinary bladder dysfunction

An excitatory role for peripheral EP3 receptors in bladder afferent function

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Prostaglandin E₂ release from isolated bladder strips in rats with spinal cord injury

An excitatory role for peripheral EP₃ receptors in bladder afferent function