Purpose: We investigated the inhibition of the contractile responses of hum
an continent and unstable detrusor muscle by the beta2 agonist clenbuterol
as well as the inhibition of electrical field stimulation evoked contractil
e responses of isolated rat bladder muscle strips by orally administered cl
enbuterol.
Materials and Methods: The contractile responses of human continent and uns
table detrusor muscle strips to electrical field stimulation (0.05 millisec
onds, 0.5 to 80 Hz.) were measured before and after adding 10(-9) to 10(-4)
M. clenbuterol in vitro. In addition, 6 rats per group were dosed orally w
ith 2 mug. kg.(-1) clenbuterol daily acutely (1 dose) or chronically (1 dos
e daily for 8 days), or with distilled water to serve as controls. The cont
ractile response to electrical field stimulation of strips of isolated detr
usor muscle was then measured. Serum clenbuterol levels were analyzed in du
plicate by enzyme-linked immunosorbent assay and high performance liquid ch
romatography.
Results: In vitro clenbuterol significantly inhibited the electrical field
stimulation evoked contractile responses of detrusor muscle strips from uns
table but not continent human bladders. A significant inhibitory effect of
clenbuterol on the electrical field stimulation evoked contractile response
of rat detrusor muscle was observed after chronic but not acute oral dosin
g (p <0.01). Serum clenbuterol levels measured by enzyme-linked immunosorbe
nt assay and high performance liquid chromatography were not significantly
different.
Conclusions: Clenbuterol or related beta2-adrenoceptor agonists may represe
nt a useful therapeutic strategy for detrusor muscle overactivity.