抄録
Normal lower urinary tract function consists of voiding and storage. During voiding, the pontine micturition reflex center orders the sacral parasympathetic nucleus to increase parasympathetic activity, resulting in urinary bladder detrusor contraction via activation of post-synaptic muscarinic receptors (M2/3), and the relaxation of both urethral and prostatic smooth muscle by NO. In addition, the rhabdosphincter relaxes by inhibition of pudendal nucleus at the sacral portion. During the storage phase, an increase in sympathetic activity relaxes urinary bladder via activation of post-synaptic β3 receptors, and both the urethral and prostatic smooth muscles are contracted via α1-adrenoceptor. Many factors influence voiding function, including lower urinary tract disorders (benign prostatic hyperplasia in males, urethral stricture), and neurological disorders (central and peripheral). Theories of action of pharmacotherapy for voiding dysfunction are: 1) increase detrusor contractility, and 2) decrease urethral resistance. The former includes agonists for muscarinic receptors, and choline-esterase inhibitor, and the latter includes α1-adrenoceptor antagonists, nitric oxide donors, Benzodiazepines, Baclofen, Dantrolene, and Boturinum toxin.
