We investigated the effect of
tamsulosin, an alpha(1)-adrenoceptor antagonist, 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 effect on intraurethral pressure response in anesthetized rats. In obstructed rats, the alpha(1)-adrenoceptor antagonists
tamsulosin,
naftopidil and
urapidil and non-selective alpha-
adrenoceptor antagonist
phentolamine inhibited premicturition contractions in a dose-dependent fashion. In contrast,
yohimbine, an alpha(2)-adrenoceptor antagonist, and
atropine, a
muscarinic receptor antagonist, hardly inhibited them.
Tamsulosin and
urapidil showed clearly inhibitory effects on increases in intraurethral pressure induced by
phenylephrine, an alpha(1)-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 conclusion, premicturition contractions observed in obstructed rats were sensitive to alpha(1)-adrenoceptor antagonists, but not to alpha(2)-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 partly support the fact that
tamsulosin has improved storage symptoms as well as voiding symptoms in patients with
lower urinary tract symptoms associated with
bladder outlet obstruction by blocking alpha(1)-adrenoceptors.