1995 Volume 31 Issue 4 Pages 119-127
Clenbuterol (10-10-10-7 M), a selective β2-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 Achinduced 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 β-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.
