|Authors||Bjorling DE, Saban MR, Saban R|
|Journal||J. Urol. Volume: 158 Issue: 1 Pages: 258-64|
|Publish Date||1997 Jul|
Somatostatin has been demonstrated to inhibit inflammation under certain circumstances. We hypothesized that in vivo treatment with octreotide, a long-acting analogue of somatostatin analogue, would diminish the capacity of inflammatory peptides to stimulate in vitro release of inflammatory mediators by the bladder.Female guinea pigs were injected with octreotide (20 mg./kg. i.m.) prior to euthanasia. Control guinea pigs received no treatment prior to euthanasia. Urinary bladders were removed and incubated with substance P (SP, 10 microM), neurokinin A (NKA, 10 microM), or bradykinin (BK, 10 microM) in the presence or absence of indomethacin (50 microM), and release of histamine, prostaglandins (PGE2 and PGF2 alpha), and leukotriene (LTB4) was determined.Sensory peptides and BK induced time-dependent release of histamine and eicosanoids from isolated urinary bladder. Blockade of cyclooxygenase with indomethacin (50 microM) abolished peptide-induced prostaglandin release but enhanced LTB4 release. In vivo octreotide pretreatment decreased peptide-induced histamine release, had no effect on PGE2 or PGF2 alpha release, and LTB4 release. However, octreotide prevented the increase in LTB4 release in tissues incubated with indomethacin.These results indicate that somatostatin has the capacity to suppress the release of histamine and prevents potentiation of LTB4 release by indomethacin by the guinea pig bladder in response to pro-inflammatory peptides, indicating that somatostatin may be useful in preventing or treating some forms of cystitis.