Colorectal distension enforce acute urinary bladder distension-induced hepatic vasoconstriction in the rat.

Acute urinary bladder distension (AUBD) and colorectal distension (CRD) activated mechanical afferents from the urinary bladder and colon and the activated afferent signaling affected visceral organ behavior. AUBD and CRD have been reported to affect the arterial blood pressure (ABP) response in the rat. We hypothesized that AUBD and CRD may influence the cardiovascular response in the liver by neurokinin receptor-mediated afferent transmission and sympathetic nerve-mediated vesicovascular reflex. We simultaneously evaluated the bladder and colorectal pressure, hepatic microcirculation and arterial blood pressure (ABP) in response to AUBD (0-60mmHg) and/or CRD stimulation (0-80mmHg) in the urethane anesthetized rat. Hepatic sympathetic denervation and intravenous CP96,345 (neurokinin 1 receptor antagonist) and SR48968 (neurokinin 2 receptor antagonist) were adopted to determine the possible neural pathways in response to AUBD and/or CRD stimulation. Our results showed that AUBD or CRD evoked a pressor response in ABP and a hepatic vasoconstriction in a pressure-dependent manner. The pressor response was demonstrated in an order AUBD>AUBD+CRD>CRD. The hepatic vasoconstrictor response was displayed in an order AUBD+CRD>AUBD>CRD. Hepatic sympathetic denervation and CP96,345 (neurokinin 1 receptor antagonist), not SR48968 (neurokinin 2 receptor antagonist), significantly inhibited AUBD, CRD and AUBD+CRD induced hepatic vasoconstriction. CRD significantly inhibited AUBD evoked spontaneous bladder contractions and ABP elevation. In conclusion, our results indicated that AUBD and CRD via neurokinin 1 receptors activate hepatic sympathetic nerve-mediated vesicovascular reflex and consequently lead to hepatic vasoconstriction. CRD exerts different cross-talk effects to influence AUBD-evoked bladder contractions and vesicovascular reflex.