The current study was undertaken in an attempt to characterize the functional properties of urothelial α 1A adrenergic receptors, especially in modulating the micturition reflex. The expression of α 1A receptors in rat bladder was analyzed by immunohistochemistry and Western blotting. As a functional study, we obtained continuous infusion cystometrograms in conscious rats using noradrenaline (NA) and subtype selective α 1 adrenergic receptor antagonists, tamsulosin (α 1A /α 1D selective) and silodosin (α 1A superselective). α 1A receptors were immunohistochemically detected in rat urothelium. Intravesical infusion of NA (60 μM) significantly shortened the intercontraction interval (ICI). Pretreatment with tamsulosin at a dose of 0.4 μg/kg i.v. abolished intravesical NA infusioninduced reduction of ICI. Neither intravesical infusion of tamsulosin (20 μM) nor that of silodosin (0.2 μM) significantly altered ICI. After intravesical infusion of silodosin, intravesical NA infusion did not affect ICI. Urothelial α 1A receptors might modulate bladder afferent activity under pathophysiological conditions with augmented concentrations of NA in blood or urine. α 1 adrenergic receptor antagonists have been the predominant form of medical therapy for the treatment of lower urinary tract symptoms in benign prostatic hyperplasia (BPH) (17). α 1 blockers were initially designed to improve voiding symptoms in BPH such as hesitancy and slow urinary flow, since α 1A adrenergic receptors enhance prostatic and urethral smooth muscle contraction to increase the resistance of urinary outflow. It turned out later that this therapy is also effective for storage symptoms such as frequency and urgency (8), suggesting the existence of another target mechanism of these drugs different from releasing bladder outlet obstruction (18). α 1 adrenergic receptors have been found at various sites in the nervous system controlling the bladder function. Intrathecal injection of α 1 antagonist increased the bladder capacity and decreased the vesical pressure during bladder contraction in rats (15, 16). In the parasympathetic ganglia of cats, α 1 antagonist prazosin inhibited the hypogastric nerveinduced facilitation of cholinergic transmission (19). In addition to their presence in the nervous system, all three subtypes of α 1 adrenergic receptors (α 1A , α 1B and α 1D ) have been identified in human and rat bladder (13,21,24). The functions of the three different subtypes in nerves and the urinary bladder were not studied until recently due to a lack of specific antagonists for each receptor subtype. The urothelium has been appreciated to be a potential modulator of bladder sensory systems because of its neuron-like properties capable of detecting mechanical or chemical stimuli and releasing a number of signaling molecules (7). The urothelial cells express diverse sensor molecules including transient receptor potential (TRP) channels (5, 6), amiloride/mechanosensitive Na + channels (ENaC) (12), receptors for purines (20,25) and acetylcho-