Effects of clenbuterol on rabbit vesicourethral muscle contractility

Clenbuterol (10(-10)-10(-7) M), a selective beta 2-adrenoceptor agonist, reduced spontaneous contractile force of isolated rabbit bladder dome, bladder base and proximal urethra. Clenbuterol inhibited both acetylcholine (Ach)-and electrical field stimulation (EFS)-induced contractions of rabbit bladder dome, but was more potent in inhibiting EFS-than Ach-induced contractions. Acetylcholine-but not EFS-induced contractions in the bladder dome were completely inhibited by pretreatment with 10(-6) M atropine. The atropine resistant component of the EFS-induced contractions was completely inhibited by tetrodotoxin, 10(-6) M. Clenbuterol and a non-selective beta-adrenoceptor agonist, isoproterenol, potentiated the EFS-induced contractions of isolated striated muscle preparations from the external urethral sphincter and from the extensor digitorum longus in the rabbit. Clenbuterol was more potent than isoproterenol in increasing EFS-induced contractile force in the external urethral sphincter, whereas isoproterenol was more potent than clenbuterol in increasing EFS-induced contractile force in the extensor digitorum longus. These data suggest that clenbuterol may have a role in the treatment of urinary incontinence by inhibiting the detrusor contraction and fascilitating the external urethral sphincter selectively.