BACKGROUND: Bombesin (BOM) and gastrin releasing peptide (GRP) have been located to the lower urinary tract. However, there is a paucity of data demonstrating the impact of these neuropeptides. OBJECTIVES: The present study investigates the impact of BOM and GRP in the female Sprague-Dawley rats 225 g b.w. n = 37 urethras in vitro and in vivo. Intraurethral pressure was recorded by a catheter placed at the maximum pressure zone corresponding to the intrinsic urethral spincter. MEASUREMENTS: In vitro, the intraurethral pressure was measured in response to the administration of BOM and GRP and noradrenaline from perfused intact urethral/bladder preparations. In vivo, changes in intraurethral pressure were conducted in anesthetized subjects and compared with the basal intraurethral pressure and sham controls. RESULTS: In vitro, the increase in intraurethral pressure induced by BOM was 23.6 ± 3.2 cmH(2) O, exceeding the pressure evoked with NA by 10.7 cmH(2) O whereas GRP induced 10.7 ± 1.6 cmH(2) O, an increase of 3.3 cmH(2) O but less than the NA evoked intraurethral pressure by 2.2 cmH(2) O. Incubation with scopolamine (1 µM), phentolamine (1 µM), pancuronium (1 µM), and indomethacin (1 µM) did not produce any significant difference in the contractile responses to BOM or GRP. In vivo, the mean basal pressure was 22.9 ± 1.4 cmH(2) O. The intraurethral pressure evoked by BOM was 29.7 cmH(2) O (21.3 ± 1.3 to 51.0 ± 1.6 cmH(2) O), and for GRP, the evoked intraurethral pressure was 33.8 cmH(2) O (22.3 ± 1.9 to 56.2 ± 30 cmH(2) O). CONCLUSIONS: BOM and GRP may contribute to the control of continence by their contractile action on the sphincters of the lower urinary tract outflow region.
BACKGROUND: Bombesin (BOM) and gastrin releasing peptide (GRP) have been located to the lower urinary tract. However, there is a paucity of data demonstrating the impact of these neuropeptides. OBJECTIVES: The present study investigates the impact of BOM and GRP in the female Sprague-Dawley rats 225 g b.w. n = 37 urethras in vitro and in vivo. Intraurethral pressure was recorded by a catheter placed at the maximum pressure zone corresponding to the intrinsic urethral spincter. MEASUREMENTS: In vitro, the intraurethral pressure was measured in response to the administration of BOM and GRP and noradrenaline from perfused intact urethral/bladder preparations. In vivo, changes in intraurethral pressure were conducted in anesthetized subjects and compared with the basal intraurethral pressure and sham controls. RESULTS: In vitro, the increase in intraurethral pressure induced by BOM was 23.6 ± 3.2 cmH(2) O, exceeding the pressure evoked with NA by 10.7 cmH(2) O whereas GRP induced 10.7 ± 1.6 cmH(2) O, an increase of 3.3 cmH(2) O but less than the NA evoked intraurethral pressure by 2.2 cmH(2) O. Incubation with scopolamine (1 µM), phentolamine (1 µM), pancuronium (1 µM), and indomethacin (1 µM) did not produce any significant difference in the contractile responses to BOM or GRP. In vivo, the mean basal pressure was 22.9 ± 1.4 cmH(2) O. The intraurethral pressure evoked by BOM was 29.7 cmH(2) O (21.3 ± 1.3 to 51.0 ± 1.6 cmH(2) O), and for GRP, the evoked intraurethral pressure was 33.8 cmH(2) O (22.3 ± 1.9 to 56.2 ± 30 cmH(2) O). CONCLUSIONS: BOM and GRP may contribute to the control of continence by their contractile action on the sphincters of the lower urinary tract outflow region.