The angiotensin II receptors type 1 blockage affects the urinary bladder activity in hyperosmolar-induced detrusor overactivity in rats: Preliminary results.

Abstract

Angiotensin II receptors play a role in the pathogenesis of urinary bladder dysfunction, especially in the case of bladder outlet obstruction. The function of these receptors in the detrusor overactivity (DO) still remains unclear. The study aims to investigate some of the mechanisms through which hyperosmolarity induces urinary bladder overactivity. The effect of angiotensin II receptor type 1 - AT1 (telmisartan) on urinary bladder function in physiological state and in hyperosmolar-induced DO in rat model was explored. Experiments were performed on 32 female Wistar rats. DO was induced by hyperosmolar saline intravesical instillation. Surgical procedures and cystometry were performed under urethane anesthesia. The measurements represent the average of 5 bladder micturition cycles. We analyzed: basal pressure, threshold pressure, micturition voiding pressure, intercontraction interval, compliance, functional bladder capacity, motility index and detrusor overactivity index. Intravesical hyperosmolar saline instillation induced DO. Telmisartan diminished the severity of hyperosmolar-induced DO. We observed a statistically significant increase of intercontraction interval (55%), functional bladder capacity (54%), compliance (140%). Also, a statistically significant decrease of detrusor overactivity index (18%) and motility index (9%) were observed. The difference of basal pressure, threshold pressure and micturition voiding pressure were not statistically significant. Moreover, telmisartan has no effect on urodynamic parameters in naïve rats. Detrusor overactivity due to intravesical increased osmolarity seems to be at least partially mediated by AT1 receptors activity. On one hand, telmisartan diminished the severity of hyperosmolarinduced DO, and, on the other hand, has no effect on urodynamic parameters in naïve rats.