{'fraction_non_alphanumeric': 0.026053639846743294, 'fraction_numerical': 0.013026819923371647, 'mean_word_length': 6.175824175824176, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The involvement of urothelial alpha1A adrenergic receptor in controlling the micturition reflex.

The current study was undertaken in an attempt to characterize the functional properties of urothelial alpha1A adrenergic receptors, especially in modulating the micturition reflex. The expression of alpha1A 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 alpha1 adrenergic receptor antagonists, tamsulosin (alpha1A/alpha1D selective) and silodosin (alpha1A superselective). Alpha1A receptors were immunohistochemically detected in rat urothelium. Intravesical infusion of NA (60 microM) significantly shortened the intercontraction interval (ICI). Pretreatment with tamsulosin at a dose of 0.4 microg/kg i.v. abolished intravesical NA infusioninduced reduction of ICI. Neither intravesical infusion of tamsulosin (20 microM) nor that of silodosin (0.2 microM) significantly altered ICI. After intravesical infusion of silodosin, intravesical NA infusion did not affect ICI. Urothelial alpha1A receptors might modulate bladder afferent activity under pathophysiological conditions with augmented concentrations of NA in blood or urine.