2010
DOI: 10.1016/j.autneu.2010.02.006
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Correlation between pharmacologically-induced changes in cystometric parameters and spinal c-Fos expression in rats

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Cited by 10 publications
(13 citation statements)
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“…This pattern was very similar to results in resiniferatoxin‐treated rats . While the mechanism of the beta‐3 AR agonist treatments are different from the resiniferatoxin treatments, a common feature of the two is the increase of urine storage. Thus, the partial reduction in the cold stress‐induced detrusor overactivity might be caused by the relaxation of the urinary detrusor promoted by CL316243.…”
Section: Discussionsupporting
confidence: 79%
“…This pattern was very similar to results in resiniferatoxin‐treated rats . While the mechanism of the beta‐3 AR agonist treatments are different from the resiniferatoxin treatments, a common feature of the two is the increase of urine storage. Thus, the partial reduction in the cold stress‐induced detrusor overactivity might be caused by the relaxation of the urinary detrusor promoted by CL316243.…”
Section: Discussionsupporting
confidence: 79%
“…Moreover, acute intraventricular and intrathecal administration of tamulosin, significantly inhibited reflex voiding in the normal rat [54] and chronic systemic treatment with two different a1-AR antagonists-inhibited reflex voiding in a rat model of BOO [55]. A recent experimental study by Nagabukuro et al [56] investigated changes in afferent firing following treatment with a number of commonly used clinical drugs. The study found that tamulosin treatment significantly attenuated activation of the early gene c-fos, commonly used as a marker for sensory neuronal activation, in the spinal cord.…”
Section: Adrenoreceptorsmentioning
confidence: 96%
“…Cystometry was performed as described previously (Nagabukuro et al, 2010). In brief, animals were anes-…”
Section: Methodsmentioning
confidence: 99%
“…Two other studies also showed a bladder capacity increase with atropine in either conscious or anesthetized rhesus monkeys (Craggs and Stephenson, 1985;Shoukry and Ghoniem, 1992). In contrast, many studies using either normal healthy or diseased rodent models did not show any bladder capacity increase with antimuscarinics or showed an increase only at the high doses (Sasaki et al, 1997;Angelico et al, 2005;Ohtake et al, 2007;Hegde et al, 2009;Nagabukuro et al, 2010), which were much higher than therapeutic doses. Only in certain disease models, such as cerebral infarction, did antimuscarinics, including tolterodine and solifenacin, increase bladder capacity at reasonable doses from clinical use of these drugs (Suzuki et al, 2005).…”
mentioning
confidence: 96%
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