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Background Overactive bladder (OAB) is described as urgency with or without incontinence, usually accompanied by frequency and nocturia. Overactive bladder reflects involuntary DSM as a consequence of enhanced cholinergic-mediated contractions and decreased b-adrenoceptor-mediated relaxations. The nitric oxide (NO)-cyclic GMP signaling pathway has been described to modulate the muscular tone, neurotransmission and blood flow in DSM, but the exact role of NO in the bladder is not completely understood. It is accepted that NO deficiency contributes to triggering OAB. The compound BAY 41–2272 has been described as a drug that directly activates the soluble guanylate cyclase leading to NO-independent cGMP accumulation. BAY 41–2272 produces potent relaxations in vascular and non-vascular smooth muscle tissues by cGMP-dependent and independent mechanisms, but no studies have been carried out with DSM.

Relaxant effect of BAY 41–2272 in the rabbit isolated detrusor smooth muscle (DSM): involvement of cGMP-independent mechanisms