Abstract
We studied that effect of intravesical administration of noradrenaline (NA) for micturition reflex in alpha1A-knockout (KO) mice and alpha1D-KO mice using the filling cystometry(CMG). Urinary bladder was infused with saline(0.4ml/h) or NA (1μg-100μg/ml). NA (10μg/ml) infusion in WT (wild type) mice shortened ICI (intercontraction interval) from 649s to 391s (60% of control, P<0.05, n=7). But NA did not altered ICI in alpha1A-KO mice (from 1047s to 1044s, 99.7%, n=7) or alpha 1D KO mice (from 663s to 746s,113%, n=7). NA shortened ICI in WT mice dose dependent fashion (1μg-100μg/ml,n=5). NA did not altered MVP (maximal voiding pressure) in WT mice, alpha1A-KO mice or alpha1D-KO mice. Intravesical administration of NA did not facilitate micturition reflex in alpha1A-KO mice and in alpha1D-KO mice. ICI in alpha 1A-KO mice was longer than WT mice or alpha1D-KO mice. Silodosin (selective alpha1A-adrenocepter antagonist) infusion followed by NA infusion did not altered the ICI from 363s to 370s (101% of control, n=4). Alpha1A-receptor and alpha1D-receptor in urothelium could activated by NA and facilitate the micturition reflex in mice. These data suggest that NA might cause hyper refexia in micturition pathway. [J Physiol Sci. 2008;58 Suppl:S154]
