Rat: Overview and innervation

Steers, William D.

doi:10.1002/nau.1930130204

Cited by 33 publications

(17 citation statements)

References 86 publications

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“…This is the first study to systematically characterize the urodynamic changes induced by social stress and to provide evidence for a putative neural mechanism. Cystometry revealed overactive detrusor and pathology similar to that produced by partial bladder outlet obstruction (42). However, unlike partial bladder obstruction, micturition pressure was not elevated, suggesting that the stress-related urinary retention resulted from a decreased drive to the bladder rather than increased outflow resistance.…”

Section: Discussionmentioning

confidence: 88%

Social stress-induced bladder dysfunction: potential role of corticotropin-releasing factor

Wood¹,

Baez²,

Bhatnagar³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

109

131

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Wood SK, Baez MA, Bhatnagar S, Valentino RJ. Social stress-induced bladder dysfunction: potential role of corticotropin-releasing factor. Am J Physiol Regul Integr Comp Physiol 296: R1671-R1678, 2009. First published May 11, 2009 doi:10.1152/ajpregu.91013.2008.-Psychological stress can impact on visceral function with pathological consequences, although the mechanisms underlying this are poorly understood. Here we demonstrate that social stress produces marked changes in bladder structure and function. Male rats were subjected to repeated (7 days) social defeat stress using the resident-intruder model. Measurement of the voiding pattern indicated that social stress produced urinary retention. Consistent with this, bladder size was increased in rats exposed to social stress. Moreover, this was negatively correlated to the latency to assume a subordinate posture, implying an association between passive behavior and bladder dysfunction. In vivo cystometry revealed distinct changes in urodynamic function in rats exposed to social stress, including increased bladder capacity, micturition volume, intermicturition interval, and the presence of non-micturition-related contractions, resembling overactive bladder. In contrast to social stress, repeated restraint (7 days) did not affect voiding, bladder weight, or urodynamics. The stress-related neuropeptide corticotropin-releasing factor (CRF) is present in spinal projections of Barrington's nucleus that regulate the micturition reflex and has an inhibitory influence in this pathway. Social stress, but not restraint, increased the number of CRF-immunoreactive neurons in Barrington's nucleus. Additionally, social stress increased CRF mRNA in Barrington's nucleus. Together, the results imply that social stress-induced CRF upregulation in Barrington's nucleus neurons results in urinary retention and, eventually, bladder dysfunction, perhaps as a visceral component of a behavioral coping response. This mechanism may underlie dysfunctional voiding in children and/or contribute to the development of stress-induced bladder disorders in adulthood.Barrington's nucleus; social defeat; micturition; cystometry; resident intruder CHRONIC OR REPEATED STRESS has numerous adverse psychological and physiological consequences (33). The mechanisms by which stress produces adverse effects have been studied in rodents using a variety of stressors. However, many of these stressors lack ethological validity (i.e., footshock). One stressor that is more ethologically relevant and is currently being used to model stress-related pathology involves social defeat (44). This model, in which a rodent is forced into submission by a larger male conspecific, has been used by several groups to examine behavioral and endocrine consequences of social stress (3,17,24,39,44). A visceral effect of social stress that is often reported, but has not been systematically investigated, is urinary retention that can develop into bladder hypertrophy and even nephropathy due to reflux (10,16,29). The neural processes t...

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Section: Discussionmentioning

confidence: 88%

Social stress-induced bladder dysfunction: potential role of corticotropin-releasing factor

Wood¹,

Baez²,

Bhatnagar³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

109

131

View full text Add to dashboard Cite

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“…Dox treatment resulted in a limited improvement in the response to FS compared with the vehicle treated. Because the response to FS is a measure of the magnitude of denervation present [Seki et al, 1992;Steers, 1994], this may indicate that the level of denervation induced by partial outlet obstruction was somewhat less severe in the dox-treated group than in vehicle-treated animals.…”

Section: Discussionmentioning

confidence: 92%

Effect of Doxazosin on rat urinary bladder function after partial outlet obstruction

Das

Leggett

Whitbeck

et al. 2002

Neurourology and Urodynamics

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Hypoxia induced by partial outlet obstruction is believed to play a major role in both the hypertrophic and degenerative effects of partial outlet obstruction. Doxazosin (dox) is a clinically effective alpha-adrenergic antagonist used in the treatment of symptomatic benign prostatic hyperplasia (BPH). Although the major therapeutic effect of the agent is believed to occur on the smooth muscle components of the prostate by reducing prostatic urethral resistance and thus improving emptying, dox may have part of its clinical action via effects mediated by other actions, including via spinal alpha-adrenergic receptors or direct effects on the bladder, possibly via inhibition of vascular alpha receptors. The specific aim of the current study was to determine whether dox pretreatment on rats affects blood flow to the bladder and reduces the level of bladder dysfunction induced by partial outlet obstruction. In part 1, eight rats were separated into two groups of four rats each. Group 1 received oral administration of dox (30 mg/kg) for 4 weeks; group 2 received vehicle (5% dimethyl sulfoxide). After 4 weeks of treatment, blood flow studies were performed using fluorescent microspheres and the bladders excised, frozen, and submitted to Interactive Medical Technologies (IMT) for blood flow analysis. In part 2, 32 adult male rats were separated into four groups of eight rats each. Groups 1 and 2 received oral administration of dox (30 mg/kg) for 4 weeks, groups 3 and 4 received vehicle (5% dimethyl sulfoxide). At 4 weeks, the rats in groups 1 and 3 received partial outlet obstructions and treatment continued for an additional 2 weeks. After 6 weeks of treatment (total), each rat was anesthetized, the bladder excised, weighed, and isolated strips mounted and contractility studies performed. 1) Four weeks pretreatment of rats with dox increased blood flow to the bladder in both the control and obstructed groups. 2) Partial outlet obstruction induced a mild decrease in blood flow. 3) The magnitude of the increased bladder weight in the vehicle-treated obstructed group was significantly greater than in the dox-treated obstructed group. 4) Partial outlet obstruction resulted in significant decreases in the contractile response to field stimulation in both treated and non-treated rats. The magnitude of the decreased response was significantly greater in the non-treated rats. 5) The response to potassium chloride was significantly reduced by partial outlet obstruction in the vehicle-treated group but not in the dox-treated group. 6) The time to maximal tension was significantly increased in response to carbachol, adenosine triphosphate, and potassium chloride. However, the magnitude of the increase was significantly greater for the vehicle-treated obstructed groups stimulated by potassium chloride than for the dox-treated groups. Dox treatment of rats increased blood flow to the bladder and reduced the severity of the response to partial outlet obstruction. These beneficial effects would be due to pharmacological effects on alph...

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“…Both species respond similarly (qualitatively) to bladder outlet partial obstruction with progressive increases in bladder mass resulting from hypertrophy and hyperplasia, as well as increased wall thickness and decreased bladder compliance [for reviews, see 3,4,22,23]. Both species respond with progressive contractile dysfunctions and increased incidence of hyperreflexia and unstable bladder contractions [3,4,23,24].…”

Section: Discussionmentioning

confidence: 99%

“…Numerous published studies using these animals provide detailed information on their normal micturition, in vivo bladder function, in vitro bladder contractile function, bladder morphology, and cellular biochemistry [for reviews, see [1][2][3]. In addition, specific models of bladder dysfunction have been created with both species [1][2][3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Rabbit versus Rat Urinary Bladder: Effects of in vitro Hypoxia

Whitbeck

Barreto²,

Horan³

et al. 1999

Pharmacology

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Purpose: Studies indicate that bladder hypoxia may be an etiological factor for lower urinary tract dysfunction. Rat and rabbit are two species of experimental animals used frequently to study lower urinary tract function and dysfunction. The objective of this study was to compare directly effects of in vitro hypoxia on contractile responses of rat and rabbit urinary bladder to different forms of stimulation. Methods: Sexually mature male New Zealand White rabbits and Sprague-Dawley rats were compared. Each bladder was excised while the animal was anesthetized, and longitudinal bladder strips were cut, then mounted in organ baths. A tension of 2 g was placed on all strips. Effects of 1, 2, 3 and 4 h hypoxia followed by 1 h of reoxygenation on contractile responses of bladder strips to field stimulation (FS), carbachol (100 μmol/l), ATP (1 mmol/l) and KCl (120 mmol/l) were determined. Results: Contractility, per unit tissue mass, of rat bladder strips was significantly greater than that of rabbit bladder strips in response to FS (all frequencies), carbachol, KCl and ATP. Hypoxia (followed by reoxygenation) resulted in time-dependent progressive reduction in contractile responses of bladder strips to all stimuli. Rat bladder was significantly more sensitive to hypoxia than rabbit bladder in response to FS and carbachol. Hypoxia induced similar effects on rat and rabbit bladder responses to ATP and KCl. Conclusion: Rat bladder neurogenic and cholinergic responses are significantly more sensitive to hypoxia than are those of rabbit bladder, which may be due to the rat bladder’s greater contractile force generation and previously reported higher Ca²⁺-ATPase activity.

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Rat: Overview and innervation

Cited by 33 publications

References 86 publications

Social stress-induced bladder dysfunction: potential role of corticotropin-releasing factor

Social stress-induced bladder dysfunction: potential role of corticotropin-releasing factor

Effect of Doxazosin on rat urinary bladder function after partial outlet obstruction

Rabbit versus Rat Urinary Bladder: Effects of in vitro Hypoxia

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