Neuropeptides and urinary bladder ischemia-reperfusion injury

Urinary bladder decompensation following partial bladder obstruction is directly related to decreased tissue perfusion, resulting in periods of hypoxia and ischemia. Hence, it is important to look for substances which could counteract against the ischemia/reperfusion- induced neuronal damage in detrusor muscle and in such a way to ameliorate the functional disorders of urinary bladder. Many neuropeptides have been found to be synthesized, stored and released in the lower urinary tract. Some of them were reported to reduce ischemia-reperfusion injury. The purpose of this study was to examine the efficacy of vasoactive intestinal peptide (VIP), somatostatin and Sandostatin® (Novartis) to counteract the damage suffered by neurons in urinary bladder exposed in vitro to experimentally induced ischemia-reperfusion in guinea-pig. We found that VIP (0.3 μM), somatostatin (300 nM) and sandostatin (1 to 300 nM) improved significantly the response to electrical field stimulation during reperfusion as compared to the control, utreated tissues. The antioxidant activity of VIP, somatostatin and sandostatin, assessed as their capability to scavenge peroxyl radicals during linoleic acid oxidation corresponded to 6.4 ± 0.1, 6.7 ± 0.3 and 7.0 ± 0.6, respectively. The antioxidant activity of the above mentioned peptides could underlie their neuroprotective action during reperfusion, when a significant amount of free radicals has been formed.