Contractile activity of the bladder urothelium/lamina propria and its regulation by nitric oxide
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In the bladder, nitric oxide (NO) is released from neuronal and non-neuronal sources, but its actions are unclear. Strips of urothelium plus lamina propria contract in response to agonists and develop spontaneous phasic contractions, and the aim of this study was to investigate the influence of NO on this activity. Isolated strips of urothelium/lamina propria from porcine bladder developed spontaneous contractions (3.5 +/- 0.3 cycles/min) and contracted in response to carbachol and electrical field stimulation (EFS). The NO synthase inhibitor N-omega-nitro-L-arginine (L-NNA, 100 mu M) had no effects on the tissues, but the NO donors diethylamine NONOate (DEANO, 100 mu M) and nitroprusside (10 mu M) caused relaxation, slowed the spontaneous rate of contractions and inhibited responses to carbachol. Maximum tonic contractions to carbachol were reduced by 17 +/- 4% (P
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