Pathways Involving Beta-3 Adrenergic Receptors Modulate Cold Stress-Induced Detrusor Overactivity in Conscious XXXX .

@entity35 @entity20105
OBJECTIVE: To investigate pathways involving beta-3 adrenergic receptors (ARs) in detrusor overactivity induced by cold stress, we determined if the beta-3 AR agonist @entity20105 could modulate the cold stress-induced detrusor overactivity in normal @entity35 . METHODS: Two   days prior to cystometric investigations, the bladders of 10-week-old female @entity35 were cannulated. Cystometric measurements of the unanesthetized, unrestricted @entity35 were taken to estimate baseline values at room temperature (RT, 27        2     C) for 20   min. They were then intravenously administered vehicle, 0.1, or 1.0   mg/kg @entity20105 (n   =   6 in each group). Five   minutes after the treatments, they were gently and quickly transferred to the low temperature (LT, 4        2     C) room for 40   min where the cystometric measurements were again made. Afterward, the @entity35 were returned to RT for final cystometric measurements. The cystometric effects of @entity20105 were also measured at RT (n   =   6 in each group). RESULTS: At RT, both low and high dose of @entity20105 decreased basal and micturition pressure while the high dose (1.0   mg/kg) significantly increased voiding interval and bladder capacity. During LT exposure, the high dose of @entity20105 partially reduced cold stress-induced detrusor overactivity characterized by increased basal pressure and urinary frequency. The high drug dose also significantly inhibited the decreases of both voiding interval and bladder capacity compared to the vehicle- and low dose (0.1   mg/kg)-treated @entity35 . CONCLUSION: A high dose of the beta-3 agonist @entity20105 could modulate cold stress-induced detrusor overactivity. Therefore, one of the mechanisms in cold stress-induced detrusor overactivity includes a pathway involving beta-3 ARs.
