Lipopolysaccharide increases agonist‐induced contractile responses in Sprague Dawley rat corpus cavernosum

Abstract

Chronic inflammatory conditions are frequent co‐morbidities of erectile dysfunction (ED) and elevated lipopolysaccharide (LPS) levels may increase inflammation via Toll‐like receptor 4 (TLR4) activation. An imbalance between vascular dilatation and contraction underlies ED. We hypothesized that LPS increases the agonist‐induced contractile response in corpus cavernosum (CC). The CC tissues were isolated, incubated for 6 hours in tissue culture media with 1 ug/mL LPS or vehicle, before being mounted in a muscle strip myograph for studies of isometric force generation. Contraction to 120 mM KCl did not differ between LPS and vehicle treated CC. KCl‐induced contraction data were used to normalize contraction data from the serotonin concentration response curve (30 nM‐100 uM). The CC tissue exposed to LPS exhibited enhanced contraction to serotonin (as % of KCl contraction) compared to control values. At 30 uM concentration: 67.34±5.15 vs. 43.34±6.67% (p<0.05), and at 100 uM: 77.61±5.4 vs. 56.61±6.98% (p<0.05). These results show that treatment with the TLR4 ligand LPS increased the contractile response to serotonin in rat corpus cavernosum. Thus, TLR4 activation may play a role in the etiology of ED which is a condition that has been shown to predict cardiovascular disease.Support: NIH and SMSNA.