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薬理と治療
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Abstract
We investigated the effects of tamsulosin and other α1−adrenoceptor antagonists on bladder function, especially spontaneous bladder contractions before micturition(premicturition contraction), in conscious rats with bladder outlet obstruction induced by partial urethral ligation, and compared the results with the effects on intraurethral pressure response in anesthetized rats. In obstructed rats, α1−adrenoceptor antagonists tamsulosin, naftopidil, silodosin and urapidil and non−selective α−adrenoceptor antagonist phentolamine inhibited premicturition contractions in a dose−dependent fashion. In contrast, yohimbine, an α2−adrenoceptor antagonist, and atropine, a muscarinic receptor antagonist, hardly inhibited them. Moreover, tamsulosin and urapidil showed clearly inhibitory effects on increases in intraurethral pressure induced by phenylephrine, an α1−adrenoceptor agonist, in the same dose range as that at which they inhibited premicturition contractions, whereas naftopidil required somewhat higher doses to inhibit increases in intraurethral pressure than those at which it inhibited premicturition contractions. In contrast, silodosin required higher doses to inhibit premicturition contractions than those at which it inhibited increases in intraurethral pressure. In conclusion, premicturition contractions observed in obstructed rats were sensitive to α1−adrenoceptor antagonists, but not to α2−adrenoceptor or muscarinic receptor antagonists. Tamsulosin was shown to be effective against both premicturition contraction and intraurethral pressure response in the same dose range in rats. These results support the fact that tamsulosin has improved storage symptoms as well as voiding symptoms in patients with bladder outlet obstruction by blocking α1−adrenoceptors. (Jpn Pharmacol Ther 2008;36:381−92)KEY WORDS Tamsulosin, Naftopidil, Silodosin, Urapidil, α1−adrenoceptor, Intraurethral pressure, Premicturition contraction, Bladder outlet obstruction
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