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Evaluation of the Potential Inhibitory Effects of Medications for Detrusor Overactivity on Platelet-Activating Factor (PAF)-Induced Mechanical Activity in Guinea Pig Bladder Smooth Muscle
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DOI：10.1248/bpb.b25-00432.png)
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Abstract
En 中文
This study aimed to determine whether currently available medications for detrusor overactivity (DO) can inhibit the platelet-activating factor (PAF)-induced increase in the mechanical activity of the urinary bladder smooth muscle (UBSM) in guinea pigs. Ten clinically used DO drugs-oxybutynin, tolterodine, fesoterodine, propiverine, propantheline, solifenacin, imidafenacin, flavoxate, urapidil, and clenbuterol- were tested at a concentration of 10 mu M, exceeding typical therapeutic plasma levels. Among these, oxybutynin exerted the most pronounced inhibitory effect, reducing the PAF (1 mu M)-induced increase in basal tone by approximately 60%. Furthermore, oxybutynin (10 mu M) also decreased 60mM KCl-induced contractions by a similar extent and nearly abolished acetylcholine (ACh, 10 mu M)-induced contractions. These findings suggest that oxybutynin suppresses PAF-induced UBSM hyperactivity through a mechanism distinct from its anticholinergic effect, likely mediated by blockade of voltage-dependent Ca2+ channels (VDCCs).
Keywords:
oxybutynin
platelet-activating factor (PAF)
voltage-dependent Ca2+ channel (VDCC)
guinea pig urinary bladder
overactive bladder (OAB)
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