Angiotensin II plays a role in acute murine experimental autoimmune cystitis BJU INTERNATIONAL Phull, H., Salkini, M., Purves, T., Funk, J., Copeland, D., Comiter, C. V. 2007; 100 (3): 664-667


To investigate whether angiotensin II (AII) receptor antagonism decreases the inflammation and oedema in acute murine experimental autoimmune cystitis (EAC), as interstitial cystitis (IC) might have an autoimmune component and AII has been implicated in autoimmune-mediated vascular congestion, oedema and scarring.Female Balb/cAN mice were divided into three treatment groups (eight in each group) that were autoimmunized with bladder homogenate to induce EAC. One group received an AII type 1 receptor (AT(1)) antagonist, one group an AII type 2 receptor (AT(2)) antagonist, and one group remained untreated (EAC). A control and sham-injected group were also included. After 10 weeks, bladders were removed, sectioned, and stained with haematoxylin and eosin.Grossly, there was no thickening or adhesions in the bladders of the control or sham-injected mice. In five of seven surviving EAC bladders, there were dense adhesions to surrounding peritoneal structures. There were also adhesions and bladder thickening in all of the AT(2) antagonist-treated mice (though in a milder form) but in only two of seven surviving AT(1) antagonist-treated mice. There was no inflammation or oedema in the sham and control groups. All the EAC bladders were inflamed, with submucosal oedema and urothelial detachment from the lamina propria. In the AT(1) antagonist-treated mice there was no inflammation or oedema. By contrast, all AT(2) antagonist-treated mice had moderate inflammation and minor detachment of the urothelium from the lamina propria.AT(1) receptor blockade ameliorated the inflammatory infiltration, submucosal oedema, and urothelial detachment associated with EAC in mice. This was achieved to a lesser extent by AT(2) receptor blockade. If some patients with IC have a pathophysiology similar to that of EAC mice, there might be potential benefit from AII receptor blockade.

View details for DOI 10.1111/j.1464-410X.2007.07035.x

View details for Web of Science ID 000248523000042

View details for PubMedID 17550411