An enhanced urethral closure reflex via the spinal cord is related to urethral resistance elevation during increased abdominal pressure. However, with the exception of monoamines, neurotransmitters modulating this reflex are not understood. We investigated whether the vasopressin V1A receptor (V1AR) is involved in the urethral closure reflex in urethane-anesthetized female rats. V1AR mRNA was highly expressed among the vasopressin receptor family in the total RNA purified from lamina IX in the spinal cord L6–S1 segment. In situ hybridization analysis of the spinal L6–S1 segment confirmed that these positive signals from the V1ARs were only detected in lamina IX. Intrathecally injected Arg8-vasopressin (AVP), an endogenous ligand, significantly increased urethral resistance during an intravesical pressure rise, and its effect was blocked by the V1AR antagonist. AVP did not increase urethral resistance in rats in which the pelvic nerves were transected bilaterally. Urethral closure reflex responses to the intravesical pressure rise increased by up to threefold compared with the baseline response after AVP administration in contrast to no increase by vehicle. In addition, intravenously and intrathecally injected V1AR antagonists decreased urethral resistance. These results suggest that V1AR stimulation in the spinal cord enhances the urethral closure reflex response, thereby increasing urethral resistance during an abdominal pressure rise and that V1AR plays a physiological role in preventing urine leakage.
Oxytocin Reduces Intravesical Pressure in Anesthetized Female Rats: Action on Oxytocin Receptors of the Urinary Bladder