Age-related differential susceptibility to calcium channel blocker and low calcium medium in rat detrusor muscle: Response to field stimulation

Yu, Hong‐Jeng; Wein, Alan J.; Levin, Robert M.

doi:10.1002/(sici)1520-6777(1996)15:5<563::aid-nau12>3.0.co;2-i

Cited by 20 publications

(11 citation statements)

References 29 publications

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“…Thus P2X receptors can be desensitized through repeated application of ␣,␤-MeATP (15). Additionally, there is always a small residual NANC component of detrusor contraction that is not mediated by either M or P2X receptors (22,56).…”

Section: Discussioncontrasting

confidence: 47%

Alterations in neurogenically mediated contractile responses of urinary bladder in rats with diabetes

Liu¹,

Daneshgari

2005

American Journal of Physiology-Renal Physiology

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Diabetic bladder dysfunction (DBD) is among the most common and bothersome complications of diabetes mellitus. Autonomic neuropathy has been counted as the cause of DBD. In the present study, we compared the alterations in the neurogenically mediated contractile responses of urinary bladder in rats with streptozocin-induced diabetes, 5% sucrose-induced diuresis, and age-matched controls. Male Sprague-Dawley rats were divided into three groups: 9-wk diabetic rats, diuretic rats, and age-matched controls. Micturition and morphometric characteristics were evaluated using metabolic cage and gross examination of the bladder. Bladder detrusor muscle strips were exposed to either periodic electrical field stimulation (EFS) or to EFS in the presence of atropine, alpha,beta-methylene adrenasine 5'-triphosphate, or tetrodotoxin. The proportions of cholinergic, purinergic, and residual nonadrenergic-noncholinergic (NANC) components of contractile response were compared among the three groups of animals. Diabetes caused a significant reduction of body weight compared with diuresis and controls, although the bladders of diabetic and diuretic rats weighed more than the controls. Both diabetes and diuresis caused significant increase in fluid intake, urine output, and bladder size. Diabetes and diuresis caused similarly increased response to EFS and reduced response to cholinergic component compared with controls. However, the purinergic response was significantly smaller in diuretic bladder strips compared with controls but not in diabetic rats. A residual NANC of unknown origin increased significantly but differently in diabetics and diuretics compared with controls. In conclusion, neurogenically mediated bladder contraction is altered in the diabetic rat. Diabetic-related changes do not parallel diuretic-induced changes, indicating that the pathogenesis of DBD needs further exploration.

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Section: Discussioncontrasting

confidence: 47%

Alterations in neurogenically mediated contractile responses of urinary bladder in rats with diabetes

Liu¹,

Daneshgari

2005

American Journal of Physiology-Renal Physiology

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“…In addition, aged rats exhibit reduced sensitivity of pelvic nerve afferents in response to increased bladder volume, but not pressure, and a reduction in the maximal bladder pressure generated during pelvic nerve stimulation (275) although the frequency-response curve for electrically evoked contractions of bladder muscle strips is similar in young and old rat bladders (725). A significant linear reduction in the amount of AChE-positive nerves was observed with increasing age in the human bladder (233), suggesting a reduced parasympathetic innervation of the aged bladder.…”

Section: Agingsupporting

confidence: 94%

Neural Control of the Lower Urinary Tract

2009

Encyclopedia of Neuroscience

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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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“…This could account for the decreased contraction in response to depolarization and to cholinergic stimulation. A previous report in rat aged detrusor shows that both contraction in response to nerve stimulation and Ca 2+ signals display a higher sensitivity to experimental inhibition of Ca 2+ influx (Yu et al 1996), in keeping with our finding.…”

Section: Discussionmentioning

confidence: 99%

“…This signalling system is directly determined by transport through plasma membrane (Ca 2+ influx channels and active Ca 2+ extrusion) and by uptake and release from intracellular Ca 2+ stores. Aging increases the dependence of detrusor contraction on extracellular Ca 2+ influx (Yu et al 1996), reduces Ca 2+ extrusion mechanisms (Gomez-Pinilla et al 2007b), and alters Ca 2+ -dependent and independent contraction pathways . However, there is no information regarding the involvement of these disturbances in the contraction changes observed in aged detrusor.…”

Section: Introductionmentioning

confidence: 99%

Aging differentially modifies agonist-evoked mouse detrusor contraction and calcium signals

Gomez‐Pinilla

Pozo

Camello

2010

AGE

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Although aging-induced changes in urinary bladder neurotransmission have been studied in some detail, information regarding alterations in detrusor muscle is scanty and addresses only partial aspects of the myogenic response of detrusor. Rodent bladder aging shows several features similar to those reported in humans. The aim of this study was to characterize in aged mouse the alterations of detrusor muscle contraction and the putative underlying changes in Ca(2+) signals. We studied in vitro the myogenic contraction induced by agonists in detrusor strips from adult (3 months old) or aged (23-25 months old) mice. In addition, we determined the agonist-induced [Ca(2+)](i) signals by epifluorescence microscopy in fura-2 loaded isolated detrusor cells. Aging impaired the contractile response of bladder strips to cholinergic stimulation with bethanechol and to chemical depolarization with KCl-containing solutions. On the contrary, the response to purinergic stimulation (ATP) was enhanced. Aging also diminished the transient Ca(2+) signal evoked by bethanechol and the Ca(2+) influx induced by KCl in bladder strips. Treatments aimed to release calcium from intracellular stores (caffeine and a low level of ionomycin in Ca(2+)-free medium) showed that aging reduces the size of agonist-releasable stores. Similar to contraction, the mobilization of Ca(2+) by ATP was increased in aged cells. Therefore, the differential effects of aging on detrusor contraction are associated to alterations of [Ca(2+)](i) signals: the cholinergic inhibition is due to inhibition of voltage-operated Ca(2+) influx and reduction of the size of intracellular Ca(2+) stores, while the age-induced ATP response is accompanied by an enhanced Ca(2+) mobilization.

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Age-related differential susceptibility to calcium channel blocker and low calcium medium in rat detrusor muscle: Response to field stimulation

Cited by 20 publications

References 29 publications

Alterations in neurogenically mediated contractile responses of urinary bladder in rats with diabetes

Alterations in neurogenically mediated contractile responses of urinary bladder in rats with diabetes

Neural Control of the Lower Urinary Tract

Aging differentially modifies agonist-evoked mouse detrusor contraction and calcium signals

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