Outflow obstruction induces changes in muscarinic and adrenergic receptor functions, and in non-adrenergic, non-cholinergic (NANC) mechanisms relevant for detrusor contraction and relaxation. The complexity of the muscarinic regulation of detrusor function makes the relative importance of the different muscarinic receptor subtypes difficult to assess, both in the normal and obstructed detrusor. This means that the optimal profile of subtype selectivity of antimuscarinic drugs meant for treatment of detrusor overactivity still remains to be established. In most animal species, detrusor contraction is mediated by both muscarinic and NANC mechanisms. The most likely transmitter responsible for the NANC-component of contraction is ATP. NANC-components are probably of minor importance in the normal human detrusor. However, if the importance of the ATP-dependent component of contraction increases in the obstructed detrusor, this may have therapeutic implications. In normal human detrusor, alpha-adrenoceptors seem to have no significant role in the contractile activation. However, the effectiveness of alpha-adrenoceptor antagonists on storage symptoms, and, occasionally, on urodynamically proven detrusor instability, in patients with outflow obstruction, suggests an involvement of alpha-adrenoceptors. The functional importance of beta-adrenoceptors for the obstructed detrusor function remains to be settled. In outflow obstruction, changes in the excitability of the detrusor smooth muscle may occur that predisposes for detrusor overactivity. Drugs acting at K+ channels can decrease detrusor excitability, and may, if cardiovascular side effects can be avoided, represent a novel, promising way of treating detrusor overactivity.